PATIENT PRESENTATION A 10-year-old African-American boy presented with multiple monomorphic papules on his forehead for 5 weeks. He denied any pruritus or tenderness over the papules. Six weeks prior to presentation, the patient was hospitalized for respiratory arrest during status asthmaticus. During his 8-day hospitalization, he underwent intubation and was treated with ampicillin, azithromycin, amoxicillin-clavulanate, dexamethasone and prednisone. The patient developed multiple papules on his forehead on hospital day 4. Nearly 1 week following discharge, the patient was prescribed clindamycin phosphate 1% solution twice daily by his primary physician. He applied the prescribed topical preparation for 4 days without improvement. His past medical history is significant for sick euthyroid and metabolic syndrome. On physical examination, the patient had multiple 1-mm to 2mm tan-white monomorphic papules on his forehead. No comedones were appreciated. The remainder of the face was unaffected, and no other suspicious areas were noted. The patient had no palpable anterior or posterior cervical lymphadenopathy.
WHAT IS YOUR DIAGNOSIS?
Diagnosis: Pityrosporum Folliculitis This case demonstrates a rare case of Pityrosporum folliculitis (PF) on the face of a 10-year old boy. PF presents predominantly on the chest, back, upper arms, and less often on the face.1-3 Criteria for diagnosis of PF include characteristic morphology, demonstration of Pityrosporum yeast in smear and/or biopsy or yellow-green Wood’s light fluorescence of the papules, and prompt response to antifungal treatment. 4 As depicted in the clinical photo above, the primary lesions of PF are monomorphic dome-shaped, follicular, erythematous, 2-mm to 3-mm papules and/or pustules.5 PF most commonly affects young and middle-aged adults and is often mistaken for acne. Furthermore, both PF and acne may occur simultaneously.1 However, in contrast to acne, and in this case, the lesions are monomorphic and comedones are not seen. Direct visualization under microscopy reveals round yeast cells and sometimes even hyphae to support the diagnosis. Ten percent KOH preparation is a fast and effective methodology for visualizing the yeast. However, the authors prefer to use chlorazol black E (CBE), a chitin-specific stain applied in the same manner as a standard 10% KOH, to highlight the spore and hyphae walls for ease in diagnosis. As depicted in Figure 1, a CBE preparation was performed and revealed multiple round spores and hyphae. For more difficult clinical cases with non-revealing KOH preparation, biopsy may be performed. Abundant round budding yeast cells and occasionally hyphae are seen in a dilated follicle (see Figure 2, a 4-mm punch biopsy from a different patient revealing spores).
PATHOPHYSIOLOGY Malassezia furfur (Pityrosporum ovale), a dimorphic lipophilic yeast, exists as normal skin flora that thrives on sebaceous skin. M furfur is thought to be involved in the pathogenesis of PF and other disorders, such as seborrheic dermatitis, tinea versicolor, and atopic dermatitis.2,3,6-10 The pathophysiology behind PF involves follicular occlusion followed by overgrowth of the yeast. As M furfur overgrows, triglycerides in the sebaceous glands are hydrolyzed into fatty acids. This triggers a cell-mediated response and activation of the alternative complement pathway causing inflammation and subsequent follicular rupture.1-3,11 Several factors can promote the overgrowth of M Furfur, such as decreased immunity caused by diabetes, cancer, HIV infection, and corticosteroid or immunosuppressive therapies. PF has a higher prevalence in immunosuppressed patients and a higher occurrence rate on the face than other areas of the body.12 Increased sebum production caused by hormonal changes, like those seen in pregnancy, can also promote PF. Products that occlude hair follicles, — such as sunscreens, cosmetics, or any other greasy substance — promote M Furfur growth, as do tight clothing and hot, humid environments. The lower incidence on the face of immunocompetent patients could be due to the lower temperature and humidity of the face in comparison with other covered parts of the body. Other notable causes of PF include stress, oral contraceptive use, and obesity. Similarly, antibiotic use decreases the amount of bacterial flora competing on the skin’s surface and accelerates M Furfur growth.2,3,7,13
DIFFERENTIAL DIAGNOSIS The differential diagnosis of PF includes acne vulgaris and steroid acne. Differentiating between them is important, as traditional acne therapies — especially antibiotics — worsen PF. Steroid Acne Steroid acne can occur in patients treated with either systemic or topical steroids. Like PF, steroid acne tends to be monomorphic and pruritic. Yu et al reported 76% of patients diagnosed as having steroid acne actually had PF.7 No improvement or worsening of symptoms with traditional acne therapy is a clue to the diagnosis of PF.
Acne Vulgaris In contrast to acne vulgaris, the papules and pustules of PF are very monomorphic and one does not see comedones or cystic lesions. Patients may also experience significant pruritus over the papules, particularly with exertion or heat. Clinical morphology and distribution are important in differentiating these conditions and presentation may differ in immunouppressed patients. PF has even been reported on the scalp, as well as the face, chest, and upper back of a 34-year-old HIV patient.12
DIAGNOSTIC METHODS Direct visualization of the yeast may be performed by multiple methods. Ten percent KOH or CBE preparation can be performed by gently scraping one of the pustules with a sterile #15 blade, smearing the contents on a glass slide, and applying 1 or 2 drops of 10% KOH or CBE and a coverslip. The slide can then be examined under a microscope and diagnosis made by visualizing multiple spores and sometimes hyphae. Culture may be helpful, but the culture media requires the addition of olive oil and is not readily available at most laboratories. Histologic examination is diagnostic, showing multiple round spores and sometimes hyphae within dilated hair follicles with keratin plugging and an inflammatory infiltrate.2 The yeast are seen in the central and deep follicle and are most dense in the ostium and pilary canal. Hematoxylin and eosin staining is usually sufficient for diagnosis. PAS and Grocott-Gomori methenamine-silver stains aid by highlighting the yeast, but are not necessary for visualization. PAS stains the spores, but not hyphae. Methylene blue and Parker ink have also been used to detect M Furfur.2
TREATMENT Treatment should include both anti-mycotic therapy and correcting predisposing factors for Malassezia overgrowth. Both topical and systemic anti-mycotic therapies may be used in managing PF. A course of both oral and topical ketoconazole is the current recommended therapy.14,15 Oral antifungals are the most effective and often lead to a rapid and dramatic resolution.6 Topical therapies are less effective in the initial treatment of PF, but are important in maintenance and prophylaxis.1 Topicals that may be used for maintenance include ciclopirox and econazole creams, as well as selenium sulfide shampoo. As mentioned previously, traditional acne therapies are not effective. Comedones are not a component of PF, therefore retinoids are not recommended. Oral antibiotics may cause flaring of PF as they inhibit competing skin flora. Therefore, discontinuation of antibiotic therapy in antibiotic-associated cases may lead to faster resolution. Additionally, altering growth promoting environments prevents recurrence.
Resolution of This Case In this case, the diagnosis — based on a forehead lesion — was confirmed by clinical morphology, direct visualization of spores and hyphae on microscopy with CBE, and resolution of the papules with a course of fluconazole 150 mg daily for 7 days. No recurrence has been noted since the short course of fluconazole.
SUMMARY Malassezia organisms have been found on 75% to 98% of healthy individuals.1,2,7 With widespread antibiotic use, incidence of PF may be on the rise. Consequently, Pityrosporum folliculitis should remain in the differential diagnosis of acneiform eruptions. As in our case, failure of acne to improve on traditional therapy may be a clue to the diagnosis. Ten percent KOH preparation (or CBE as in this case) with microscopy is usually sufficient for diagnosis. Rapid resolution with anti-mycotic therapy confirms the diagnosis. However, histopathological examination is also diagnostic and may be performed on clinically suspicious lesions.
Dr. Sage is with the Department of Dermatology, Henry Ford Health System, Detroit, MI. Marian Ibrahim is a medical student at the Wayne State University School of Medicine, Detroit, MI. Dr. Ozog in private practice in Detroit and is also affiliated with the Department of Dermatology, Henry Ford Health System, Detroit, MI. Dr. Khachemoune, the Section Editor of Derm Dx, is with Department of Dermatology, State University of New York, Brooklyn, NY.
Disclosure: The authors have no conflicts of interest with any material presented in this column.
References 1. Ayers K, Sweeney SM, Wiss K. Pityrosporum folliculitis: diagnosis and management in 6 female adolescents with acne vulgaris. Arch Pediatr Adolesc Med. 2005;159:64-67.
2. Gupta AK, Batra R, Bluhm R, et al. Skin diseases associated with Malassezia species. J Am Acad Dermatol. 2004;51:785-798.
3. Archer-Dubon C, Icaza-Chivez ME, Orozco-Topete R, et al. An epidemic outbreak of Malassezia folliculitis in three adult patients in an intensive care unit: a previously unrecognized nosocomial infection. Int J Dermatol. 1999;38:453-456.
4. James WD, Berger TG, Elston DM. Diseases resulting from fungi and yeasts. Andrews’ Disease of the Skin Clinical Dermatology (10th ed). Philadelphia: Elsevier; 2006. p. 297-332.
5. Janik MP and Heffernan PR. Yeast infections: candidiasis and tinea (pityriasis) versicolor. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick’s Dermatology in General Medicine (7th ed). New York: McGraw Hill; 2008. p. 1822-1830.
6. Faergemann J, Bergbrant IM, Dohse M, et al. Seborrheic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry. Br J Dermatol. 2000;144:549-556.
7. Yu HJ, Lee SK, Son SJ, et al. Steroid acne vs. Pityrosporum folliculitis: the incidence of Pityrosporum ovale and the effect of antifungal drugs in steroid acne. Int J Dermatol. 1998;37:772-777.
8. Savolainen J, Lintu P, Kosonen J, et al. Pityrosporum and Candida specific and non-specific humoral, cellular, and cytokine responses in atopic dermatitis patients. Clin Exp Allergy. 1999;31:125-134.
9. Devos SA, van der Valk PGM. The relevance of skin prick tests for Pityrosporum ovale in patients with head and neck dermatitis. Allergy 2000;55:1056-1058.
10. Lintu P, Savolainen OK, Kalimo K, et al. Cross reacting IgE and IgG antibodies to Pityrosporum ovale mannan and other yeasts in atopic dermatitis. Allergy. 1999;54:1067-1073.
11. Leeming JP, Notman FH, Holland KT. The distribution and ecology of Malassezia furfur and cutaneous bacteria on human skin. J Appl Bacteriol. 1989;67:47-52.
12. Budavari JM, Grayson W. Papular follicular eruptions in human immunodeficiency virus-positive patients in South Africa. Int J Dermatol. 2007;46:706-710.
13. Le Gal FA, Zylberberg H, Zylberberg L, et al. Deep necrotizing Pityrosporum folliculitis in a HIV-positive patient. Int Conf AIDS. 1994;10;159.
14. Hill MK, Goodfield JD, Rodgers FG, Crowley JL, Saihan EM. Skin surface electron microscopy in Pityrosporum folliculitis. The role of follicular occlusion in disease and the response to oral ketoconazole. Arch Dermatol. Feb 1990; 126(2): 181-4.
15. Ford GP, Ive FA, Midgley G. Pityrosporum folliculitis and ketoconazole. Br J Dermatol. Dec 1982;107(6):691-5.
PATIENT PRESENTATION A 10-year-old African-American boy presented with multiple monomorphic papules on his forehead for 5 weeks. He denied any pruritus or tenderness over the papules. Six weeks prior to presentation, the patient was hospitalized for respiratory arrest during status asthmaticus. During his 8-day hospitalization, he underwent intubation and was treated with ampicillin, azithromycin, amoxicillin-clavulanate, dexamethasone and prednisone. The patient developed multiple papules on his forehead on hospital day 4. Nearly 1 week following discharge, the patient was prescribed clindamycin phosphate 1% solution twice daily by his primary physician. He applied the prescribed topical preparation for 4 days without improvement. His past medical history is significant for sick euthyroid and metabolic syndrome. On physical examination, the patient had multiple 1-mm to 2mm tan-white monomorphic papules on his forehead. No comedones were appreciated. The remainder of the face was unaffected, and no other suspicious areas were noted. The patient had no palpable anterior or posterior cervical lymphadenopathy.
WHAT IS YOUR DIAGNOSIS?
Diagnosis: Pityrosporum Folliculitis This case demonstrates a rare case of Pityrosporum folliculitis (PF) on the face of a 10-year old boy. PF presents predominantly on the chest, back, upper arms, and less often on the face.1-3 Criteria for diagnosis of PF include characteristic morphology, demonstration of Pityrosporum yeast in smear and/or biopsy or yellow-green Wood’s light fluorescence of the papules, and prompt response to antifungal treatment. 4 As depicted in the clinical photo above, the primary lesions of PF are monomorphic dome-shaped, follicular, erythematous, 2-mm to 3-mm papules and/or pustules.5 PF most commonly affects young and middle-aged adults and is often mistaken for acne. Furthermore, both PF and acne may occur simultaneously.1 However, in contrast to acne, and in this case, the lesions are monomorphic and comedones are not seen. Direct visualization under microscopy reveals round yeast cells and sometimes even hyphae to support the diagnosis. Ten percent KOH preparation is a fast and effective methodology for visualizing the yeast. However, the authors prefer to use chlorazol black E (CBE), a chitin-specific stain applied in the same manner as a standard 10% KOH, to highlight the spore and hyphae walls for ease in diagnosis. As depicted in Figure 1, a CBE preparation was performed and revealed multiple round spores and hyphae. For more difficult clinical cases with non-revealing KOH preparation, biopsy may be performed. Abundant round budding yeast cells and occasionally hyphae are seen in a dilated follicle (see Figure 2, a 4-mm punch biopsy from a different patient revealing spores).
PATHOPHYSIOLOGY Malassezia furfur (Pityrosporum ovale), a dimorphic lipophilic yeast, exists as normal skin flora that thrives on sebaceous skin. M furfur is thought to be involved in the pathogenesis of PF and other disorders, such as seborrheic dermatitis, tinea versicolor, and atopic dermatitis.2,3,6-10 The pathophysiology behind PF involves follicular occlusion followed by overgrowth of the yeast. As M furfur overgrows, triglycerides in the sebaceous glands are hydrolyzed into fatty acids. This triggers a cell-mediated response and activation of the alternative complement pathway causing inflammation and subsequent follicular rupture.1-3,11 Several factors can promote the overgrowth of M Furfur, such as decreased immunity caused by diabetes, cancer, HIV infection, and corticosteroid or immunosuppressive therapies. PF has a higher prevalence in immunosuppressed patients and a higher occurrence rate on the face than other areas of the body.12 Increased sebum production caused by hormonal changes, like those seen in pregnancy, can also promote PF. Products that occlude hair follicles, — such as sunscreens, cosmetics, or any other greasy substance — promote M Furfur growth, as do tight clothing and hot, humid environments. The lower incidence on the face of immunocompetent patients could be due to the lower temperature and humidity of the face in comparison with other covered parts of the body. Other notable causes of PF include stress, oral contraceptive use, and obesity. Similarly, antibiotic use decreases the amount of bacterial flora competing on the skin’s surface and accelerates M Furfur growth.2,3,7,13
DIFFERENTIAL DIAGNOSIS The differential diagnosis of PF includes acne vulgaris and steroid acne. Differentiating between them is important, as traditional acne therapies — especially antibiotics — worsen PF. Steroid Acne Steroid acne can occur in patients treated with either systemic or topical steroids. Like PF, steroid acne tends to be monomorphic and pruritic. Yu et al reported 76% of patients diagnosed as having steroid acne actually had PF.7 No improvement or worsening of symptoms with traditional acne therapy is a clue to the diagnosis of PF.
Acne Vulgaris In contrast to acne vulgaris, the papules and pustules of PF are very monomorphic and one does not see comedones or cystic lesions. Patients may also experience significant pruritus over the papules, particularly with exertion or heat. Clinical morphology and distribution are important in differentiating these conditions and presentation may differ in immunouppressed patients. PF has even been reported on the scalp, as well as the face, chest, and upper back of a 34-year-old HIV patient.12
DIAGNOSTIC METHODS Direct visualization of the yeast may be performed by multiple methods. Ten percent KOH or CBE preparation can be performed by gently scraping one of the pustules with a sterile #15 blade, smearing the contents on a glass slide, and applying 1 or 2 drops of 10% KOH or CBE and a coverslip. The slide can then be examined under a microscope and diagnosis made by visualizing multiple spores and sometimes hyphae. Culture may be helpful, but the culture media requires the addition of olive oil and is not readily available at most laboratories. Histologic examination is diagnostic, showing multiple round spores and sometimes hyphae within dilated hair follicles with keratin plugging and an inflammatory infiltrate.2 The yeast are seen in the central and deep follicle and are most dense in the ostium and pilary canal. Hematoxylin and eosin staining is usually sufficient for diagnosis. PAS and Grocott-Gomori methenamine-silver stains aid by highlighting the yeast, but are not necessary for visualization. PAS stains the spores, but not hyphae. Methylene blue and Parker ink have also been used to detect M Furfur.2
TREATMENT Treatment should include both anti-mycotic therapy and correcting predisposing factors for Malassezia overgrowth. Both topical and systemic anti-mycotic therapies may be used in managing PF. A course of both oral and topical ketoconazole is the current recommended therapy.14,15 Oral antifungals are the most effective and often lead to a rapid and dramatic resolution.6 Topical therapies are less effective in the initial treatment of PF, but are important in maintenance and prophylaxis.1 Topicals that may be used for maintenance include ciclopirox and econazole creams, as well as selenium sulfide shampoo. As mentioned previously, traditional acne therapies are not effective. Comedones are not a component of PF, therefore retinoids are not recommended. Oral antibiotics may cause flaring of PF as they inhibit competing skin flora. Therefore, discontinuation of antibiotic therapy in antibiotic-associated cases may lead to faster resolution. Additionally, altering growth promoting environments prevents recurrence.
Resolution of This Case In this case, the diagnosis — based on a forehead lesion — was confirmed by clinical morphology, direct visualization of spores and hyphae on microscopy with CBE, and resolution of the papules with a course of fluconazole 150 mg daily for 7 days. No recurrence has been noted since the short course of fluconazole.
SUMMARY Malassezia organisms have been found on 75% to 98% of healthy individuals.1,2,7 With widespread antibiotic use, incidence of PF may be on the rise. Consequently, Pityrosporum folliculitis should remain in the differential diagnosis of acneiform eruptions. As in our case, failure of acne to improve on traditional therapy may be a clue to the diagnosis. Ten percent KOH preparation (or CBE as in this case) with microscopy is usually sufficient for diagnosis. Rapid resolution with anti-mycotic therapy confirms the diagnosis. However, histopathological examination is also diagnostic and may be performed on clinically suspicious lesions.
Dr. Sage is with the Department of Dermatology, Henry Ford Health System, Detroit, MI. Marian Ibrahim is a medical student at the Wayne State University School of Medicine, Detroit, MI. Dr. Ozog in private practice in Detroit and is also affiliated with the Department of Dermatology, Henry Ford Health System, Detroit, MI. Dr. Khachemoune, the Section Editor of Derm Dx, is with Department of Dermatology, State University of New York, Brooklyn, NY.
Disclosure: The authors have no conflicts of interest with any material presented in this column.
References 1. Ayers K, Sweeney SM, Wiss K. Pityrosporum folliculitis: diagnosis and management in 6 female adolescents with acne vulgaris. Arch Pediatr Adolesc Med. 2005;159:64-67.
2. Gupta AK, Batra R, Bluhm R, et al. Skin diseases associated with Malassezia species. J Am Acad Dermatol. 2004;51:785-798.
3. Archer-Dubon C, Icaza-Chivez ME, Orozco-Topete R, et al. An epidemic outbreak of Malassezia folliculitis in three adult patients in an intensive care unit: a previously unrecognized nosocomial infection. Int J Dermatol. 1999;38:453-456.
4. James WD, Berger TG, Elston DM. Diseases resulting from fungi and yeasts. Andrews’ Disease of the Skin Clinical Dermatology (10th ed). Philadelphia: Elsevier; 2006. p. 297-332.
5. Janik MP and Heffernan PR. Yeast infections: candidiasis and tinea (pityriasis) versicolor. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick’s Dermatology in General Medicine (7th ed). New York: McGraw Hill; 2008. p. 1822-1830.
6. Faergemann J, Bergbrant IM, Dohse M, et al. Seborrheic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry. Br J Dermatol. 2000;144:549-556.
7. Yu HJ, Lee SK, Son SJ, et al. Steroid acne vs. Pityrosporum folliculitis: the incidence of Pityrosporum ovale and the effect of antifungal drugs in steroid acne. Int J Dermatol. 1998;37:772-777.
8. Savolainen J, Lintu P, Kosonen J, et al. Pityrosporum and Candida specific and non-specific humoral, cellular, and cytokine responses in atopic dermatitis patients. Clin Exp Allergy. 1999;31:125-134.
9. Devos SA, van der Valk PGM. The relevance of skin prick tests for Pityrosporum ovale in patients with head and neck dermatitis. Allergy 2000;55:1056-1058.
10. Lintu P, Savolainen OK, Kalimo K, et al. Cross reacting IgE and IgG antibodies to Pityrosporum ovale mannan and other yeasts in atopic dermatitis. Allergy. 1999;54:1067-1073.
11. Leeming JP, Notman FH, Holland KT. The distribution and ecology of Malassezia furfur and cutaneous bacteria on human skin. J Appl Bacteriol. 1989;67:47-52.
12. Budavari JM, Grayson W. Papular follicular eruptions in human immunodeficiency virus-positive patients in South Africa. Int J Dermatol. 2007;46:706-710.
13. Le Gal FA, Zylberberg H, Zylberberg L, et al. Deep necrotizing Pityrosporum folliculitis in a HIV-positive patient. Int Conf AIDS. 1994;10;159.
14. Hill MK, Goodfield JD, Rodgers FG, Crowley JL, Saihan EM. Skin surface electron microscopy in Pityrosporum folliculitis. The role of follicular occlusion in disease and the response to oral ketoconazole. Arch Dermatol. Feb 1990; 126(2): 181-4.
15. Ford GP, Ive FA, Midgley G. Pityrosporum folliculitis and ketoconazole. Br J Dermatol. Dec 1982;107(6):691-5.
PATIENT PRESENTATION A 10-year-old African-American boy presented with multiple monomorphic papules on his forehead for 5 weeks. He denied any pruritus or tenderness over the papules. Six weeks prior to presentation, the patient was hospitalized for respiratory arrest during status asthmaticus. During his 8-day hospitalization, he underwent intubation and was treated with ampicillin, azithromycin, amoxicillin-clavulanate, dexamethasone and prednisone. The patient developed multiple papules on his forehead on hospital day 4. Nearly 1 week following discharge, the patient was prescribed clindamycin phosphate 1% solution twice daily by his primary physician. He applied the prescribed topical preparation for 4 days without improvement. His past medical history is significant for sick euthyroid and metabolic syndrome. On physical examination, the patient had multiple 1-mm to 2mm tan-white monomorphic papules on his forehead. No comedones were appreciated. The remainder of the face was unaffected, and no other suspicious areas were noted. The patient had no palpable anterior or posterior cervical lymphadenopathy.
WHAT IS YOUR DIAGNOSIS?
Diagnosis: Pityrosporum Folliculitis This case demonstrates a rare case of Pityrosporum folliculitis (PF) on the face of a 10-year old boy. PF presents predominantly on the chest, back, upper arms, and less often on the face.1-3 Criteria for diagnosis of PF include characteristic morphology, demonstration of Pityrosporum yeast in smear and/or biopsy or yellow-green Wood’s light fluorescence of the papules, and prompt response to antifungal treatment. 4 As depicted in the clinical photo above, the primary lesions of PF are monomorphic dome-shaped, follicular, erythematous, 2-mm to 3-mm papules and/or pustules.5 PF most commonly affects young and middle-aged adults and is often mistaken for acne. Furthermore, both PF and acne may occur simultaneously.1 However, in contrast to acne, and in this case, the lesions are monomorphic and comedones are not seen. Direct visualization under microscopy reveals round yeast cells and sometimes even hyphae to support the diagnosis. Ten percent KOH preparation is a fast and effective methodology for visualizing the yeast. However, the authors prefer to use chlorazol black E (CBE), a chitin-specific stain applied in the same manner as a standard 10% KOH, to highlight the spore and hyphae walls for ease in diagnosis. As depicted in Figure 1, a CBE preparation was performed and revealed multiple round spores and hyphae. For more difficult clinical cases with non-revealing KOH preparation, biopsy may be performed. Abundant round budding yeast cells and occasionally hyphae are seen in a dilated follicle (see Figure 2, a 4-mm punch biopsy from a different patient revealing spores).
PATHOPHYSIOLOGY Malassezia furfur (Pityrosporum ovale), a dimorphic lipophilic yeast, exists as normal skin flora that thrives on sebaceous skin. M furfur is thought to be involved in the pathogenesis of PF and other disorders, such as seborrheic dermatitis, tinea versicolor, and atopic dermatitis.2,3,6-10 The pathophysiology behind PF involves follicular occlusion followed by overgrowth of the yeast. As M furfur overgrows, triglycerides in the sebaceous glands are hydrolyzed into fatty acids. This triggers a cell-mediated response and activation of the alternative complement pathway causing inflammation and subsequent follicular rupture.1-3,11 Several factors can promote the overgrowth of M Furfur, such as decreased immunity caused by diabetes, cancer, HIV infection, and corticosteroid or immunosuppressive therapies. PF has a higher prevalence in immunosuppressed patients and a higher occurrence rate on the face than other areas of the body.12 Increased sebum production caused by hormonal changes, like those seen in pregnancy, can also promote PF. Products that occlude hair follicles, — such as sunscreens, cosmetics, or any other greasy substance — promote M Furfur growth, as do tight clothing and hot, humid environments. The lower incidence on the face of immunocompetent patients could be due to the lower temperature and humidity of the face in comparison with other covered parts of the body. Other notable causes of PF include stress, oral contraceptive use, and obesity. Similarly, antibiotic use decreases the amount of bacterial flora competing on the skin’s surface and accelerates M Furfur growth.2,3,7,13
DIFFERENTIAL DIAGNOSIS The differential diagnosis of PF includes acne vulgaris and steroid acne. Differentiating between them is important, as traditional acne therapies — especially antibiotics — worsen PF. Steroid Acne Steroid acne can occur in patients treated with either systemic or topical steroids. Like PF, steroid acne tends to be monomorphic and pruritic. Yu et al reported 76% of patients diagnosed as having steroid acne actually had PF.7 No improvement or worsening of symptoms with traditional acne therapy is a clue to the diagnosis of PF.
Acne Vulgaris In contrast to acne vulgaris, the papules and pustules of PF are very monomorphic and one does not see comedones or cystic lesions. Patients may also experience significant pruritus over the papules, particularly with exertion or heat. Clinical morphology and distribution are important in differentiating these conditions and presentation may differ in immunouppressed patients. PF has even been reported on the scalp, as well as the face, chest, and upper back of a 34-year-old HIV patient.12
DIAGNOSTIC METHODS Direct visualization of the yeast may be performed by multiple methods. Ten percent KOH or CBE preparation can be performed by gently scraping one of the pustules with a sterile #15 blade, smearing the contents on a glass slide, and applying 1 or 2 drops of 10% KOH or CBE and a coverslip. The slide can then be examined under a microscope and diagnosis made by visualizing multiple spores and sometimes hyphae. Culture may be helpful, but the culture media requires the addition of olive oil and is not readily available at most laboratories. Histologic examination is diagnostic, showing multiple round spores and sometimes hyphae within dilated hair follicles with keratin plugging and an inflammatory infiltrate.2 The yeast are seen in the central and deep follicle and are most dense in the ostium and pilary canal. Hematoxylin and eosin staining is usually sufficient for diagnosis. PAS and Grocott-Gomori methenamine-silver stains aid by highlighting the yeast, but are not necessary for visualization. PAS stains the spores, but not hyphae. Methylene blue and Parker ink have also been used to detect M Furfur.2
TREATMENT Treatment should include both anti-mycotic therapy and correcting predisposing factors for Malassezia overgrowth. Both topical and systemic anti-mycotic therapies may be used in managing PF. A course of both oral and topical ketoconazole is the current recommended therapy.14,15 Oral antifungals are the most effective and often lead to a rapid and dramatic resolution.6 Topical therapies are less effective in the initial treatment of PF, but are important in maintenance and prophylaxis.1 Topicals that may be used for maintenance include ciclopirox and econazole creams, as well as selenium sulfide shampoo. As mentioned previously, traditional acne therapies are not effective. Comedones are not a component of PF, therefore retinoids are not recommended. Oral antibiotics may cause flaring of PF as they inhibit competing skin flora. Therefore, discontinuation of antibiotic therapy in antibiotic-associated cases may lead to faster resolution. Additionally, altering growth promoting environments prevents recurrence.
Resolution of This Case In this case, the diagnosis — based on a forehead lesion — was confirmed by clinical morphology, direct visualization of spores and hyphae on microscopy with CBE, and resolution of the papules with a course of fluconazole 150 mg daily for 7 days. No recurrence has been noted since the short course of fluconazole.
SUMMARY Malassezia organisms have been found on 75% to 98% of healthy individuals.1,2,7 With widespread antibiotic use, incidence of PF may be on the rise. Consequently, Pityrosporum folliculitis should remain in the differential diagnosis of acneiform eruptions. As in our case, failure of acne to improve on traditional therapy may be a clue to the diagnosis. Ten percent KOH preparation (or CBE as in this case) with microscopy is usually sufficient for diagnosis. Rapid resolution with anti-mycotic therapy confirms the diagnosis. However, histopathological examination is also diagnostic and may be performed on clinically suspicious lesions.
Dr. Sage is with the Department of Dermatology, Henry Ford Health System, Detroit, MI. Marian Ibrahim is a medical student at the Wayne State University School of Medicine, Detroit, MI. Dr. Ozog in private practice in Detroit and is also affiliated with the Department of Dermatology, Henry Ford Health System, Detroit, MI. Dr. Khachemoune, the Section Editor of Derm Dx, is with Department of Dermatology, State University of New York, Brooklyn, NY.
Disclosure: The authors have no conflicts of interest with any material presented in this column.
References 1. Ayers K, Sweeney SM, Wiss K. Pityrosporum folliculitis: diagnosis and management in 6 female adolescents with acne vulgaris. Arch Pediatr Adolesc Med. 2005;159:64-67.
2. Gupta AK, Batra R, Bluhm R, et al. Skin diseases associated with Malassezia species. J Am Acad Dermatol. 2004;51:785-798.
3. Archer-Dubon C, Icaza-Chivez ME, Orozco-Topete R, et al. An epidemic outbreak of Malassezia folliculitis in three adult patients in an intensive care unit: a previously unrecognized nosocomial infection. Int J Dermatol. 1999;38:453-456.
4. James WD, Berger TG, Elston DM. Diseases resulting from fungi and yeasts. Andrews’ Disease of the Skin Clinical Dermatology (10th ed). Philadelphia: Elsevier; 2006. p. 297-332.
5. Janik MP and Heffernan PR. Yeast infections: candidiasis and tinea (pityriasis) versicolor. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick’s Dermatology in General Medicine (7th ed). New York: McGraw Hill; 2008. p. 1822-1830.
6. Faergemann J, Bergbrant IM, Dohse M, et al. Seborrheic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry. Br J Dermatol. 2000;144:549-556.
7. Yu HJ, Lee SK, Son SJ, et al. Steroid acne vs. Pityrosporum folliculitis: the incidence of Pityrosporum ovale and the effect of antifungal drugs in steroid acne. Int J Dermatol. 1998;37:772-777.
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