AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

Of possible interest are eMedicine acne articles on acne, as follows:

• Acne Conglobata
• Acne Fulminans
• Acne Keloidalis Nuchae
• Acne Vulgaris
• 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 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

Section 3 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

The 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. 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. 

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. See Tinea Barbae and 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. See Gram-Negative Folliculitis. 

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. See Pseudofolliculitis of the Beard.

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. See Acne Keloidalis Nuchae.

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. 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.¹¹

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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

Laboratory studies are typically not obtained because diagnosis is usually made based on history and physical examination findings alone. In cases resistant to standard therapy, cultures, Gram stain, potassium chloride (KOH) preparation, and biopsy are the diagnostic tests of choice.

• Gram stain and bacterial culture are best performed by unroofing an entire pustule with a No. 15 blade and depositing material onto a glass slide and a sterile cotton swab. In typical cases, Gram stain shows gram-positive cocci, and culture grows S aureus. Pseudomonas species can be cultured from the pustules of hot tub folliculitis.
• Nasal culture of family members to look for S aureus colonization may be needed in chronic cases.
• KOH inspection, fungal culture, or both can be useful for diagnosing dermatophyte infections. Pityrosporum yeast forms are best appreciated on biopsy specimens in cases of Pityrosporum folliculitis
• Viral culture or biopsy assists in the identification of folliculitis caused by herpes simplex virus.
• A small punch biopsy (3-4 mm) of an active lesion should be performed in atypical cases or in patients resistant to standard treatments. Patients with eosinophilic folliculitis show eosinophils and lymphocytes within the hair follicle. A complete blood cell count often reveals leukocytosis and eosinophilia, with an elevated immunoglobulin E level.

Procedures

For deep infections, incision and drainage can be therapeutic and can provide material to be sent for culture.

Histologic Findings

Histologically, all cases of superficial folliculitis have a similar appearance in that they show a moderately intense infiltrate of inflammatory cells in the follicular ostium and upper regions of the follicle. In most cases, the inflammation initially consists of neutrophils and then becomes more mixed with the addition of lymphocytes and macrophages. If the folliculitis is from an infectious cause, then various organisms can be identified within the follicle.¹²

Folliculitis can also extend deeper, with the inflammation involving the entire length of the follicle and often encompassing the adjacent dermis as a focal dermal abscess.
 
In perifolliculitis, the inflammation is restricted to the area immediately surrounding the follicle.

The histopathological evaluation of herpes folliculitis can be subtle and nonspecific and often requires that deeper histological sections are obtained in order to see the characteristic histological changes. Typically, a dense lymphohistiocytic infiltrate is noted, often admixed with neutrophils that surround and frequently destroy the hair follicle. The characteristic changes of a herpes infection, namely balloon degeneration of the keratinocytes of the follicle, scattered multinucleated cells, and keratinocytes with enlarged gray nuclei that have peripheral margination of the chromatin, are seen in approximately half the cases on which a biopsy has been performed. Most cases of herpes folliculitis have been shown to be caused by a varicella-zoster infection, and, initially, the infection is centered on the sebaceous gland.⁹

In pseudofolliculitis barbae and acne keloidalis nuchae, the inflammatory infiltrate is initially perifollicular and is composed of neutrophils and lymphocytes; however, later, they are replaced by monocytes and plasma cells. Often, free hair shafts without the accompanying follicle can be identified within the dermis. The hair shafts are typically surrounded by acute or granulomatous inflammation and fibrosis. Hypertrophic scar is often present.¹²

The histological features of eosinophilic folliculitis include a collection of eosinophils within the superficial follicle associated with eosinophilic spongiosis and a mild perifolliculitis. This type of folliculitis is often associated with follicular mucinosis.⁵

The histological features of a papulopustular eruption due to EGF-R inhibitors is that of a superficial purulent folliculitis, which, in most cases, is sterile but can occasionally be associated with S aureus infection.²

TREATMENT

Section 6 of 11  

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• Follow-up
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Medical Care

For recurrent uncomplicated superficial folliculitis, use of antibacterial soaps and good hand washing technique may be all that is needed. For refractory or deep lesions that have a suspected infectious etiology, empiric treatment with topical and/or oral antibiotics that cover gram-positive organisms may be of benefit. If a patient does not improve with a standard course of antibiotics, other causes of folliculitis must be investigated.

If systemic antibiotics are indicated, coverage should include S aureus, because S aureus is the most common pathogen. This organism often is penicillin resistant; therefore, dicloxacillin or a cephalosporin is the first choice. Methicillin-resistant organisms are becoming more common, and treatment may require clindamycin, trimethoprim-sulfamethoxazole, minocycline, or linezolid.

For recurrent and recalcitrant folliculitis, mupirocin ointment in the nasal vestibule twice a day for 5 days may eliminate the S aureus carrier state. Family members also may be nasal carriers of S aureus, and mupirocin ointment or rifampin at 600 mg/d orally for 10 days may eliminate the carrier state.  

Medical care for the other types of folliculitis is as follows:

• Pseudomonas folliculitis is usually self-limited and does not require treatment; however, if the patient is immunocompromised or the lesions are persistent, oral ciprofloxacin may be given.
• Eosinophilic pustular folliculitis does not respond to systemic antibiotics; however, it may respond to isotretinoin, metronidazole, UV-B phototherapy, indomethacin, or itraconazole.
• Pityrosporum folliculitis initially responds to topical antifungals such as ketoconazole cream or shampoo but is often associated with relapses. For relapses, systemic antifungals should be tried.
• Herpetic folliculitis responds to valacyclovir, famciclovir, or acyclovir.
• Papulopustular eruption associated with EGF-R inhibitors is self-limited and resolves with cessation of chemotherapy. In patients requiring treatment, topical antibiotics or topical corticosteroids can be used, and, in recalcitrant cases, oral antibiotics can be administered.

Consultations

The patient's primary care provider can usually diagnose and treat uncomplicated cases of folliculitis, but for those cases that are persistent or result in scarring, a dermatologist should be consulted.

Diet

Because folliculitis is more common in individuals who are obese, weight reduction may be helpful.

Activity

If the patient equates episodes of folliculitis to wearing a wet suit or other sports gear, these items should be cleaned with antimicrobial soaps and dried well.

MEDICATION

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• Follow-up
• Miscellaneous
• Multimedia
• References

Topical antibiotics can be used as first-line agents in cases of recurrent superficial folliculitis. If the area involved is widespread or persistent or if a deep infection is present, systemic antibiotics may be indicated. The drug of choice must cover penicillin- or methicillin-resistant S aureus in areas of high prevalence or in predisposed patients.

Drug Category: Antibiotics

For patients who do not respond to standard antimicrobial treatments, therapy should be guided by culture sensitivity.

Drug Category: Antifungal agents

Many topical antifungal preparations are available to treat the forms of folliculitis (eg, tinea barbae, Pityrosporum folliculitis) caused by fungus. Topical agents should be active against dermatophytes.

Drug Category: Antiviral agents

Inhibitors of DNA polymerase in HSV-1 and HSV-2 strains, inhibiting viral replication.

FOLLOW-UP

Section 8 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
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Further Outpatient Care

Arrange a follow-up visit within 2 weeks to check response to treatment.

Deterrence/Prevention

Avoid shaving irritated skin for 1 month or until all lesions have resolved. To prevent future lesions, avoid close shaving and change disposable razors daily. In addition, periodically soak electric razor heads in 70% alcohol or diluted bleach for 1 hour to eliminate overgrowth of bacteria or fungi.

Good personal hygiene, including bathing, hand washing, and keeping nails short and clean, reduces the risk of folliculitis. Wearing loose rather than snug-fitting clothing helps reduce friction.

In cases of acute folliculitis, launder towels, washcloths, and sheets frequently and do not share them with other family members.  

Hot tubs should be cleaned regularly and appropriately chlorinated.

Complications

Persistent and deep folliculitis can result in scarring, sinus tract formation, and permanent hair loss.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

If a patient does not improve on standard antimicrobial therapy, consider other causes or resistant organisms and perform culture and biopsy as needed. Failure to treat identifiable causes of folliculitis can result in complications.

MULTIMEDIA

Section 10 of 11  

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• Multimedia
• References

Media file 1:  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.
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Media file 2:  A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.
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Media file 3:  Pseudomonas folliculitis. Courtesy of Hon Pak, MD.
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Media file 4:  Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle
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Media file 5:  Perifolliculitis, showing inflammatory cells surrounding the follicle,
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Media type:  Photo

REFERENCES

Section 11 of 11

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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. Roé E, García Muret MP, Marcuello E, Capdevila J, Pallarés 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. Böer 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. 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].
12. Weedon D, Strutton G. Skin Pathology. 2^nd ed. New York, NY: Churchill Livingstone; 2002:459-66.
13. 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].
14. Arndt KA, Robinson JK, Wintroub BU, LeBoit PE. Dermatology: Cutaneous Medicine and Surgery in Primary Care. Philadelphia, Pa: WB Saunders; 1997.
15. Bolognia JL, Jorizzo JL, Rapini RP. Dermatology. Vol 1. St. Louis, Mo: Mosby; 2003:553-66.
16. 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].

Article Last Updated: Apr 17, 2008