eMedicine Specialties > Dermatology > Diseases of the Adnexa

Folliculitis

Author: Elizabeth Kline Satter, MD, MPH, Chairman, Department of Dermatology, Naval Medical Center San Diego
Contributor Information and Disclosures

Updated: Mar 3, 2010

Introduction

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.

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

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.

Clinical

History

The folliculitis patient typically reports an acute onset of papules and pustules associated with pruritus or mild discomfort.

Patients with deep folliculitis usually experience more pain and may have suppurative drainage. Persistent or recurrent lesions may result in scarring and permanent hair loss.

The papulopustular eruption secondary to EGF-R inhibitors typically occurs within the first 2 weeks of the initiation of therapy and can be associated with pruritus, pain, and desquamation.

Physical

Patients with superficial folliculitis usually present with multiple small papules and pustules on an erythematous base that are pierced by a central hair, although the hair may not always be visualized. Deeper lesions manifest as erythematous, often fluctuant, nodules. Sometimes, a patterned folliculitis occurs in areas that were shaved or occluded. Any hair-bearing site can be affected, but the sites most often involved are the face, scalp, thighs, axilla, and inguinal area.

Folliculitis has been traditionally divided into superficial and deep forms; however, most superficial forms can evolve into the deep form. The most common superficial form of infectious folliculitis is known as impetigo of Bockhart or barbers itch and is caused by Staphylococcus aureus, such as the infection shown in the image below . The lesions are seen in the bearded area, often on the upper lip near the nose, as erythematous follicular-based papules or pustules that may rupture and leave a yellow crust. The pustule is often pierced by a hair that is easily extracted from the follicle. This form of folliculitis occurs more commonly in carriers of nasal staphylococci. Another type of superficial folliculitis caused by staphylococci is a sty, which only differs from typical folliculitis in that it occurs on the eyelid.

A 22-month-old boy with a staphylococcal follicul...

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 22-month-old boy with a staphylococcal follicul...

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.


When involvement of the follicle is more extensive, a follicular-centered dermal abscess results. When the condition occurs on the face, it is referred to as sycosis barbae (vulgaris), but if it occurs elsewhere, it is referred to as a furuncle or boil. A confluence of several furuncles results in a carbuncle.6

Tinea barbae is an uncommon form of superficial folliculitis that clinically resembles its bacterial counterpart; however, it is caused by a superficial infection by various zoophilic dermatophytes. This superficial fungal folliculitis is most commonly seen in male farmers and typically affects one side of the face in the submaxillary region or chin. Patients with more extensive involvement of the follicle or those who experience an exaggerated hypersensitivity reaction to the dermatophyte infection present with enlarged, boggy purulent plaques, called kerions, in the site of the prior superficial infection. Another deep fungal folliculitis occurs on the legs of women who shave, and this is called Majocchi granuloma.

Gram-negative folliculitis primarily occurs in patients on long-term antibiotic therapy, often antibiotics given for the treatment of acne. This type of folliculitis arises from disequilibrium of the normal skin bacteria in favor of gram-negative organisms such as Enterobacter, Klebsiella, Escherichia, Serratia, and Proteus species. These lesions manifest as multiple small pustules that are most pronounced in the perinasal region and can spread to the chin and cheeks.

Pseudomonal folliculitis is another gram-negative folliculitis and is also known as hot tub (spa) folliculitis and wet suit folliculitis (see the images below). It appears 8-48 hours after exposure to contaminated water or wet suits as erythematous follicular-based papules and pustules that are most concentrated in areas occluded by swimwear. This form of folliculitis may be associated with systemic findings such as fever, headache, sore throat, malaise, or gastrointestinal distress, but it is a self-limited condition that resolves in 7-14 days. Another similar condition is hot hand-foot syndrome, which occurs in a similar clinical situation but eventuates in painful erythematous nodules and papules on the palms and soles rather than folliculitis.7

A 30-year-old woman with hot tub folliculitis. Sh...

A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.

A 30-year-old woman with hot tub folliculitis. Sh...

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.

Pseudomonas folliculitis. Courtesy of Hon Pak, MD.

Pseudomonas folliculitis. Courtesy of Hon Pak, MD.

Pseudomonas folliculitis. Courtesy of Hon Pak, MD.


Pityrosporum folliculitis is typically seen in young adults, with a slight female predominance, as intensively pruritic small uniform papules and pustules on the back, chest, and shoulders. It occurs more often in warm, humid climates and may be more frequent in immunocompromised patients or in patients on long-term antibiotics. This eruption is due to follicular infection by Malassezia furfur, which is a lipophilic yeast.

An unusual cause of folliculitis occurs as a result of either overgrowth of Demodex mites or an acquired hypersensitivity to the mite. This form of folliculitis manifests with a more diffuse background erythema, in addition to the follicular-centered papules and pustules.8

An uncommon form of folliculitis is due to an infection with herpes viruses. This form of folliculitis can be caused by an infection by herpes simplex viruses 1 and 2 and is found in areas adjacent to a primary cold sore. It is spread by shaving. These lesions appear as grouped or scattered vesicles.9,10

Varicella-zoster virus may also cause a primarily follicular-based infection. These patients present with erythematous plaques in a dermatomal distribution; however, vesicles do not typically occur. Biopsy is often required to confirm the diagnosis.10

Folliculitis can also have a noninfectious etiology caused by follicular trauma or occlusion or may simply be idiopathic. For example, pseudofolliculitis barbae, also known as shaving or razor bumps, occurs primarily in the bearded area of African American males or other racial groups with thick, coarse, curly hair. This condition is not a folliculitis per se, but rather a perifolliculitis that arises as a result of the hair reentering the skin adjacent to its exit point from the follicle. The hair then acts as a foreign body and incites inflammation. The inflammation can spontaneously resolve if the hair is extracted or it can become associated with a chronic foreign body granulomatous reaction and may result in scarring.

Acne keloidalis nuchae is a similar condition that arises on the neck and occipital region of the scalp, but this condition is both a folliculitis and perifolliculitis and has greater potential for scarring.

Acute generalized exanthematous pustulosis and anticonvulsant hypersensitivity syndrome both manifest as an acute onset of a discrete pustular eruption arising shortly after beginning therapy with various medications. Although the eruption that occurs in acute generalized exanthematous pustulosis is often differentiated from anticonvulsant hypersensitivity syndrome by having nonfollicular-based pustules, either condition can have follicular or nonfollicular-based pustules.

Papulopustular drug eruption due to EGF-R is a relatively new entity and consists of a follicular eruption on the face, chest, and upper back that occurs approximately 2 weeks after initiation of chemotherapy. It is seen in up to 90% of patients taking EGF-R inhibitors, and its presence correlates to a positive response to chemotherapy.1,2

The last noninfectious folliculitis to be discussed is eosinophilic folliculitis. It manifests as intensely pruritic pustules and can occur in at least 3 different clinical situations. The first is the original description of eosinophilic folliculitis, also know as Ofuji disease. It arises in Japanese males at an average age of 30 years. The lesions initially begin as discrete papules and pustules that eventually coalesce to form circinate plaques composed of a peripheral rim of pustules with central clearing. These lesions appear cyclically on the face, back, and extensor surfaces of the arms and spontaneously resolve in 7-10 days. Often, peripheral eosinophilia is present.5

A second form of eosinophilic folliculitis arises in patients with AIDS and other conditions that result in immunosuppression.11 This form is seen most often in adult males with a CD4+ count of less than 300 cells/μL. It is persistent and does not form an annular pattern. The lesions tend to favor the face, scalp, and upper trunk.12

The last form of eosinophilic folliculitis occurs in infants, usually within the first 24 hours to first few weeks of life. It is more common in male infants and usually is self-limited; however, as in Ofuji disease, it may follow a cyclic course lasting months to years. The lesions primarily affect the scalp and eyebrows. This form may also be associated with peripheral eosinophilia.

Causes

The causes of folliculitis are multiple and include infection, friction and other causes of follicular trauma, excessive perspiration, and occlusion; however, many cases remain idiopathic. Patients who have a reduced immune status, prior skin injury, or dermatoses or those who are obese may be more at risk.

More on Folliculitis

Overview: Folliculitis
Differential Diagnoses & Workup: Folliculitis
Treatment & Medication: Folliculitis
Follow-up: Folliculitis
Multimedia: Folliculitis
References

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.

Further Reading

Keywords

folliculitis, superficial folliculitis, deep folliculitis, infectious folliculitis, Staphylococcus aureus, Pseudomonas, gram-negative bacteria, herpes, dermatophytes, Pityrosporum, Demodex, perifolliculitis, impetigo of Bockhart, barbers itch, sty, sycosis barbae, sycosis barbae vulgaris, furuncle, carbuncle, acute generalized exanthematous pustulosis, tinea barbae, Majocchi granuloma, kerion, eosinophilic folliculitis, pseudofolliculitis barbae, shaving bumps, razor bumps, acne keloidalis nuchae

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.

Medical Editor

Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; 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.

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

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

CME Editor

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, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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