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Pityrosporum Folliculitis Versus Acne Vulgaris: What Is Fungal Acne?

Pityrosporum folliculitis (PF), referred to colloquially as “fungal acne,” was first described in 1969 by Weary et al as an acneiform eruption associated with recent antibiotic use.1 Due to its similar appearance and distribution to Acne Vulgaris (AV), the two conditions are often confused. This leads to delayed treatment of PF and traditional acne treatments, especially antibiotics, will worsen the condition.2 The following article will explore the similarities and differences between PF and Acne Vulgaris. This is not meant to be an extensive review of AV but will provide enough information to compare and contrast these similar conditions.

Pathogenesis

Both Pityrosporum Folliculitis and Acne Vulgaris are inflammatory conditions involving the pilosebaceous unit, which involves the hair shaft, hair follicle, and sebaceous gland. The inflammation is related to a microorganism in both conditions.

Pityrosporum folliculitis 

PF is an infection of the hair follicle caused by the yeast Malessezia furfur (and possible other strains). It is a dimorphic lipophilic yeast that is part of the fungal kingdom, thus why the condition is sometimes referred to as “fungal acne.” The fungal kingdom is vast, containing as many as 5 million diverse species, including unicellular yeasts, filamentous fungi, mushrooms, and lichens.3

Malessezia furfur is extremely common, present in the stratum corneum and hair follicles in about 90% of people without PF.2 Pathogenic features of Malessezia furfur, however, involve follicular occlusion followed by overgrowth of the yeast that thrives in the sebaceous environment. Like Propionibacterium acnes, Malessezia has been shown to induce keratinocytes to generate inflammatory cytokines via Toll-like receptor 2,5, and 7.4 This may explain why PF and acne are similar in appearance.

Malessezia furfur is also the pathogen associated with tinea versicolor and seborrheic dermatitis. While these conditions are sometimes seen with PF, there is no significant association. One study found that only 15% of patients with PF had associated seborrheic dermatitis and 4% had tinea versicolor.4 Therefore, the absence of these conditions does not exclude a diagnosis of PF.

Acne vulgaris 

AV is a condition caused by chronic inflammation of the pilosebaceous unit.5 Keratinocytes within the follicle can desquamate and create a micro-comedone, which, when combined with excess sebum production during puberty, becomes the perfect environment for colonization of Propionibacterium acnes.5 This bacterium stimulates keratinocytes to release inflammatory factors which leads to the formation of typical inflammatory acne pustules, papules and comedones. The presence of comedones is a differentiating factor from PF as comedones are not present in PF.

 

Epidemiology

Pityrosporum folliculitis

According to a retrospective review of 110 patients by Prindaville et al., PF is more commonly found in females than males (69% and 31% respectively).4 It is much more common in whites (65%) than Hispanics (11%), African Americans (3%), and Asian (2%). The average age of patients with PF is 15.3. 54% of patients had previous oral antibiotic treatment, which included cephalexin, doxycycline, minocycline, trimethoprim-sulfamethoxazole, and tetracycline. Only 16% of patients were on topical clindamycin on presentation.4

PF is commonly found in adolescents presumably due to the increased activity of sebaceous glands during this time. This leads to follicular occlusion and overgrowth of the yeast that thrives in the sebaceous environment.2 It is also more common in hot and humid weather, with flares occurring in these types of climates or in the summer months.2

Acne vulgaris 

AV affects the vast majority of people between the ages of 15 and 17 and is moderate to severe in 15-20% of patients, with the severity of acne correlating with pubertal maturation. Teenage boys are more frequently affected than girls, with some estimates being that 100% of teenage boys developing some amount of acne.6 Acne Vulgaris is seen as the most common dermatological diagnosis in both black and white individuals with relatively equal prevalence. The annular percentage of referrals for AV in the United Kingdom in different racial groups was determined to be 51% black, 41% white, and 8% Asian or Arabic.7 In a large study surveying Asian patients (eg, Chinese, Malaysians, and Indians) in a Singapore clinic, it was determined that AV was the second most common diagnosis (occurring in 10.9% of the adult population8.

AV can persist into adulthood for unclear reasons, with acne continuing into the 20s-30s in 64% and 43% of individuals respectively.5 AV is strongly heritable with 80% of individuals developing the condition if a first-degree relative was/is affected. Sunlight and poor hygiene are sometimes thought to affect the severity of AV, but no association has been found.5 A recent large scale study found that consumption of dairy, sugary beverages, and fatty and sugary products is associated with current acne in adults.9

 

Clinical Presentation

Pityrosporum folliculitis 

PF presents as monomorphic 1-2mm papules and pustules (sometimes described as keratosis pilaris like) on the face, chest, and back. The most common locations are the forehead, often extending to the hairline, (74%) and the upper back (73%).4 These lesions are usually pruritic, but not always, and the absence of pruritus does not exclude the diagnosis.4 A diagnostic clue pointing towards PF in the patient’s history is minimal improvement or worsening of the rash despite the use of antibiotics for a suspected diagnosis of Acne Vulgaris. Comedones are characteristically absent in PF.

Acne vulgaris 

Acne lesions consist of comedones, inflammatory papules and pustules, nodules, and cystic lesions with distribution of the face, chest, back, and shoulders. In different age groups, some acne lesion types are more common than others.6 In neonates, comedonal acne is commonly seen on the nose, cheeks, and forehead with onset before 6 weeks of age. This is thought to be secondary to maternal and infant androgens and will usually resolve spontaneously in 1-3 months.6 Acne seen later in infancy (onset between 3 and 6 months) is much less common and predisposes the individual to develop severe acne later in life. This presents as inflammatory lesions on the face and is more commonly seen in male infants. Preteens have predominantly centrofacial comedonal acne, while teens have the typical “mixed” acne (all lesion types seen) on the face and trunk. Adult women will more commonly have inflammatory lesions located periorally and on the jawline.6 Comedones are characteristically present in acne.

The incidence of nodulocystic acne may be lower in African Americans than Caucasians and Hispanics. However, post-inflammatory hyperpigmentation (PIH) is actually much more common in dark-skinned individuals, despite appearing to have fewer inflammatory lesions.5 Interestingly, there is marked inflammation seen histologically in lesions that appear noninflammatory on dark-skinned individuals, which may play a role in the increased degree PIH seen.6

 

Diagnostics

Pityrosporum folliculitis 

PF can be diagnosed clinically, but there are several diagnostic studies available to confirm the diagnosis, including microscopic evaluation for the presence of yeast, cultures, or biopsy.10 Wood’s lamp and dermoscopy can also aid in the diagnosis. Wood’s lamp can illuminate the lesions, giving them a yellow-green florescence.10 There are also several dermascopic features that can be helpful in the diagnosis of PF.11 These include folliculocentric papules and pustules with surrounding erythema, dirty white perilesional scales, coiled/ looped hairs with perifollicular erythema and scaling, hypopigmentation of the involved hair follicles, and perilesional brownish discoloration in resolving lesions.11

Punch biopsies may be helpful. On histology, PF positive specimens will have dilated follicles plugged with keratinous material, amorphous cellular debris, and inflammatory cells. The follicle will also contain many round yeast forms and stain positive with Periodic Acid-Schiff (PAS) stain. When performing a biopsy, similarly to a KOH, it is important to obtain the follicle base to ensure a more accurate diagnosis.

Acne vulgaris 

No testing is needed to make a diagnosis, as this condition is diagnosed clinically based on the classic morphology of acne lesions.12 Biopsies and cultures are not usually recommended unless systemic infection is suspected. Work up for PF may be necessary if lesions are not responding or worsening with classic acne treatments.

Although androgens play a role in the pathogenesis of acne, most patients have normal hormone levels and there is little evidence supporting routine endocrine testing in patients presenting with acne.12

 

Treatment

Pityrosporum folliculitis 

Antifungal medications are the treatment of choice for PF. These can be used either topically or orally. Oral medications are utilizd for more widespread maintenance and prophylaxis. Medications found to be effective include: oral ketoconazole, oral fluconazole, ketoconazole 2% shampoo used as a wash, ketoconazole 2% cream, and sulfur wash.4 Since 2013, the Food and Drug Administration has cautioned against the use of oral ketoconazole for superficial fungal infections due to the risk of liver or adrenal injury. Therefore, ketoconazole is no longer recommended in the treatment of PF.4

It is important to recognize that acne vulgaris and MF often co-exist, so it may be necessary to combine antifungal treatments with typical acne medications. However, it is important to be careful when including antibiotics as this may promote further overgrowth.10 It also may be helpful to discontinue all acne medications while treating PF initially, so as to determine the extent of acne vulgaris after treatment of PF.10

Observation of what triggers flares (and avoidance of these triggers) is also important for treatment. Increased frequency of treatments may be required during summer months (when weather is hot and humid) and during periods of increased sweating, such intense exercise or outdoor work.10 Occlusive clothing and topical products, such as make-up, lotion, or sunscreen, may promote flares.10

Acne vulgaris 

Acne vulgaris is treated with numerous topical and systemic medications aimed at decreasing inflammation and increasing the turnover of keratinocytes so to “unclog” pores. Common topical medications include retinoids, benzoyl peroxide, and topical antibiotics (such as clindamycin, erythromycin, and minocycline).12

Systemic antibiotics (such as doxycycline and minocycline) are part of the current standard of care for the management of moderate to severe acne and treatment resistant forms of inflammatory acne. However, bacterial resistance to these antibiotics is becoming problematic and shorter courses are now recommended.12

Hormonal agents, such as oral contraceptives and antiandrogen agents (ie. Spironolactone), can also be used to treat acne in women.12

Lastly, oral isotretinoin is approved for the treatment of severe scarring acne or acne that is recalcitrant to other treatment options. It is extremely effective, but has a variety of side effects, most important being it teratogenicity. Women of childbearing age taking this medication must be on two forms of birth control.12

 

Comparison of Pityrosporum Folliculitis and Acne Vulgaris

 

Pityrosporum Folliculitis

Acne Vulgaris

Pathogenesis

Inflammatory conditions involving the pilosebaceous unit

Common Organism

Malessezia furfur

Propionibacterium acnes

Patient Characteristics

-Teenagers

-Females>males

-Antibiotic use prior to onset/worsening of condition is common

-Common during summer months and hot/humid climates

-Most common in pre-teens, teenagers, and young adults

-Prevalence equal in blacks and whites

Clinical Presentation

-Monomorphic 1-2mm papules and pustules

-Commonly forehead (extending to hairline), chest, and/ or back

-Commonly presents with acne vulgaris

-Pruritic (not always)

-Comedones with or without inflammatory papules and pustules of varying sizes

-Nodulocystic acne present in severe cases

-Scarring and post-inflammatory hyperpigmentation common in darker-skinned individuals

Diagnosis

-Clinically based on morphology of lesions

-Woods lamp= yellow-green florescence

-Clinically based on morphology of lesions

Treatment

-Antifungal medications: oral fluconazole, ketoconazole 2% shampoo used as a wash, ketoconazole 2% cream, and sulfur wash

-Avoid treatment with antibiotics if concomitantly treating for acne vulgaris

-Occasional use of topical antifungals likely necessary to prevent future flares

-Avoidance of triggers

-Topical retinoids, benzoyl peroxide, antibiotics

-Oral antibiotics (doxycycline, minocycline)

-Hormonally targeted therapy (oral contraceptives, spironolactone)

-Oral isotretinoin

 

Practical Tips

  • Pityrosporum folliculitis (also called “fungal acne”) commonly presents in white, female teenagers as pruritic monomorphic 1-2mm papules on the face, chest, and/or back.
  • PF often occurs concomitantly with acne.
  • PF should be considered when “acne” is not improving or worsening with classic acne medications, especially if antibiotics are being used.
  • Diagnosis of PF can be made clinically or dermoscopicly, but there are also several diagnostic tests that can be used to confirm the diagnosis, including KOH and biopsy.
  • Antifungals are the treatment of choice for PF; chronic treatment may include the use of daily topical antifungals to control/ prevent future flares.
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References

  1. Weary PE. Acneform Eruption Resulting From Antibiotic Administration. Arch Dermatol. 1969;100(2):179. doi:10.1001/archderm.1969.01610260055009
  2. Ayers K, Sweeney SM, Wiss K. Pityrosporum Folliculitis: Diagnosis and Management in 6 Female Adolescents With Acne Vulgaris. Arch Pediatr Adolesc Med. 2005;159(1):64. doi:10.1001/archpedi.159.1.64
  3. Heitman J. Microbial pathogens in the fungal kingdom. Fungal Biol Rev. 2011;25(1):48-60. doi:10.1016/j.fbr.2011.01.003
  4. Prindaville B, Belazarian L, Levin NA, Wiss K. Pityrosporum folliculitis: A retrospective review of 110 cases. J Am Acad Dermatol. 2018;78(3):511-514. doi:10.1016/j.jaad.2017.11.022
  5. Bhate K, Williams HC. Epidemiology of acne vulgaris: Epidemiology of acne vulgaris. Br J Dermatol. 2013;168(3):474-485. doi:10.1111/bjd.12149
  6. White GM. Recent findings in the epidemiologic evidence, classification, and subtypes of acne vulgaris. J Am Acad Dermatol. 1998;39(2):S34-S37. doi:10.1016/S0190-9622(98)70442-6
  7. Child, Fuller, Higgins, Du Vivier. A study of the spectrum of skin disease occurring in a black population in south-east London: SKIN DISEASE IN A BLACK POPULATION. Br J Dermatol. 1999;141(3):512-517. doi:10.1046/j.1365-2133.1999.03047.x
  8. Goh CL, Akarapanth R. Epidemiology of Skin Disease Among Children in a Referral Skin Clinic in Singapore. Pediatr Dermatol. 1994;11(2):125-128. doi:10.1111/j.1525-1470.1994.tb00565.x
  9. Penso L, Touvier M, Deschasaux M, et al. Association Between Adult Acne and Dietary Behaviors: Findings From the NutriNet-Santé Prospective Cohort Study. JAMA Dermatol. Published online June 10, 2020. doi:10.1001/jamadermatol.2020.1602
  10. Rubenstein RM, Malerich SA. Malassezia (pityrosporum) folliculitis. J Clin Aesthetic Dermatol. 2014;7(3):37-41.
  11. Jakhar D, Kaur I, Chaudhary R. Dermoscopy of pityrosporum folliculitis. J Am Acad Dermatol. 2019;80(2):e43-e44. doi:10.1016/j.jaad.2018.08.057
  12. Strauss JS, Krowchuk DP, Leyden JJ, et al. Guidelines of care for acne vulgaris management. J Am Acad Dermatol. 2007;56(4):651-663. doi:10.1016/j.jaad.2006.08.048