Folliculitis 

  • Author: Elizabeth Kline Satter, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Aug 4, 2011
 

Background

Folliculitis is defined histologically as the presence of inflammatory cells within the wall and ostia of the hair follicle, creating a follicular-based pustule. The actual type of inflammatory cells can vary and may be dependent on the etiology of the folliculitis, the stage at which the biopsy specimen was obtained, or both. The inflammation can be either limited to the superficial aspect of the follicle with primary involvement of the infundibulum or the inflammation can affect both the superficial and deep aspect of the follicle. Deep folliculitis can eventuate from chronic lesions of superficial folliculitis or from lesions that are manipulated, and this may ultimately result in scarring.

Perifolliculitis, on the other hand, is defined as the presence of inflammatory cells in the perifollicular tissues and can involve the adjacent reticular dermis. Folliculitis and perifolliculitis can manifest independently or together as a result of follicular disruption and irritation.

Acne represents a noninfectious form of folliculitis. The follicular inflammation seen in acne occurs as a secondary event as a result of follicular obstruction from abnormal keratinization. In acne, the superficial aspect of the follicle distends and is obstructed by a keratin plug. The sebum fills the follicle, and the normally commensal bacteria (Propionibacterium acnes) produces excess free fatty acids, which trigger follicular inflammation.

Acne-related eMedicine articles include Acne Conglobata, Acne Fulminans, Acne Keloidalis Nuchae, Acne Vulgaris, and Acneiform Eruptions.

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Pathophysiology

Folliculitis is a primary inflammation of the hair follicle that occurs as a result of various infections, or it can be secondary to follicular trauma or occlusion.

Eosinophilic folliculitis differs in that it is thought to occur as a result of an autoimmune process directed against the sebocytes or some component of the sebum.

Although the etiology of papulopustular eruption secondary to epidermal growth factor receptor (EGF-R) inhibitors is unknown, it is hypothesized to occur secondary to abnormal epidermal differentiation that leads to follicular obstruction and subsequent inflammation.[1, 2]

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Epidemiology

Frequency

United States

Superficial folliculitis is common, but because it is often self-limited, patients rarely present to the doctor. Those who are seen more often have either recurrent/persistent superficial folliculitis or have deep folliculitis. Although the incidence is unknown, certain conditions make patients more susceptible. These include frequent shaving, immunosuppression, preexisting dermatoses, long-term antibiotic use, occlusive clothing and/or occlusive dressings, exposure to hot humid temperatures, diabetes mellitus, obesity, and use of EGF-R inhibitor medications.

Folliculitis has been reported following smallpox or anthrax vaccine. These cases may become more common because more military troops are being deployed.[3]

Mortality/Morbidity

Although complications from folliculitis are uncommon, they include cellulitis, furunculosis, scarring, and permanent hair loss.

Race

Folliculitis occurs in persons of any race, but pseudofolliculitis and traction folliculitis occurs more commonly in African Americans and classic eosinophilic folliculitis is more common in Japanese persons.[4, 5]

Sex

For most cases of folliculitis, no data are available to indicate the presence of a sexual predilection; however, eosinophilic folliculitis is reported to more frequently affect males and Pityrosporum folliculitis may have a slightly increased female incidence.

Age

Folliculitis can be seen in persons of all ages.

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Contributor Information and Disclosures
Author

Elizabeth Kline Satter, MD, MPH  Chairman, Department of Dermatology, Naval Medical Center San Diego

Elizabeth Kline Satter, MD, MPH is a member of the following medical societies: Alpha Omega Alpha and American Medical Women's Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

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.

References
  1. Bragg J, Pomeranz MK. Papulopustular drug eruption due to an epidermal growth factor receptor inhibitors, erlotinib and cetuximab. Dermatol Online J. 2007;13(1):1. [Medline].

  2. Roe E, Garcia Muret MP, Marcuello E, Capdevila J, Pallares C, Alomar A. Description and management of cutaneous side effects during cetuximab or erlotinib treatments: a prospective study of 30 patients. J Am Acad Dermatol. Sep 2006;55(3):429-37. [Medline].

  3. Walsh SR, Johnson RP. Vaccinia Folliculitis After Primary Dryvax Vaccination. Infect Dis Clin Pract. Mar 2007;15(2):132-4.

  4. Fox GN, Stausmire JM, Mehregan DR. Traction folliculitis: an underreported entity. Cutis. Jan 2007;79(1):26-30. [Medline].

  5. Nervi SJ, Schwartz RA, Dmochowski M. Eosinophilic pustular folliculitis: a 40 year retrospect. J Am Acad Dermatol. Aug 2006;55(2):285-9. [Medline].

  6. Eley CD, Gan VN. Picture of the month. Folliculitis, furunculosis, and carbuncles. Arch Pediatr Adolesc Med. Jun 1997;151(6):625-6. [Medline].

  7. Yu Y, Cheng AS, Wang L, Dunne WM, Bayliss SJ. Hot tub folliculitis or hot hand-foot syndrome caused by Pseudomonas aeruginosa. J Am Acad Dermatol. Oct 2007;57(4):596-600. [Medline].

  8. Dong H, Duncan LD. Cytologic findings in Demodex folliculitis: a case report and review of the literature. Diagn Cytopathol. Mar 2006;34(3):232-4. [Medline].

  9. Boer A, Herder N, Winter K, Falk T. Herpes folliculitis: clinical, histopathological, and molecular pathologic observations. Br J Dermatol. Apr 2006;154(4):743-6. [Medline].

  10. Weinberg JM, Mysliwiec A, Turiansky GW, Redfield R, James WD. Viral folliculitis. Atypical presentations of herpes simplex, herpes zoster, and molluscum contagiosum. Arch Dermatol. Aug 1997;133(8):983-6. [Medline].

  11. Zancanaro PC, McGirt LY, Mamelak AJ, Nguyen RH, Martins CR. Cutaneous manifestations of HIV in the era of highly active antiretroviral therapy: an institutional urban clinic experience. J Am Acad Dermatol. Apr 2006;54(4):581-8. [Medline].

  12. Majors MJ, Berger TG, Blauvelt A, Smith KJ, Turner ML, Cruz PD Jr. HIV-related eosinophilic folliculitis: a panel discussion. Semin Cutan Med Surg. Sep 1997;16(3):219-23. [Medline].

  13. Vary JC Jr, Colven R, Kirby P. Hypertrophic scars from surgical staples mimicking folliculitis. J Am Acad Dermatol. Jan 2010;62(1):157-8. [Medline].

  14. Weedon D, Strutton G. Skin Pathology. 2nd ed. New York, NY: Churchill Livingstone; 2002:459-66.

  15. Satoh T, Shimura C, Miyagishi C, Yokozeki H. Indomethacin-induced reduction in CRTH2 in eosinophilic pustular folliculitis (Ofuji's disease): a proposed mechanism of action. Acta Derm Venereol. 2010;90(1):18-22. [Medline].

  16. Arenas R, Toussaint S, Isa-Isa R. Kerion and dermatophytic granuloma. Mycological and histopathological findings in 19 children with inflammatory tinea capitis of the scalp. Int J Dermatol. Mar 2006;45(3):215-9. [Medline].

  17. Arndt KA, Robinson JK, Wintroub BU, LeBoit PE. Dermatology: Cutaneous Medicine and Surgery in Primary Care. Philadelphia, Pa: WB Saunders; 1997.

  18. Bolognia JL, Jorizzo JL, Rapini RP. Dermatology. Vol 1. St. Louis, Mo: Mosby; 2003:553-66.

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A 22-month-old boy with a staphylococcal folliculitis on the buttocks. The lesions have been excoriated. Diaper occlusion may have been related to onset of the rash.
A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.
Pseudomonas folliculitis. Courtesy of Hon Pak, MD.
Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle
Perifolliculitis, showing inflammatory cells surrounding the follicle,
 
 
 
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