Folliculitis

Updated: Aug 05, 2024
  • Author: Elizabeth K Satter, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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Overview

Practice Essentials

Folliculitis is a relatively common condition that arises due to an accumulation of inflammatory cells within the superficial or deep aspect of the hair follicle and has either an infectious or non-infectious etiology.  Folliculitis frequently occurs as a result of minor trauma to the hair follicle, such as shaving, scratching, recurrent friction or secondary to persistent follicular occlusion which then triggers a local inflammatory response.  Damaged follicles are also more predisposed to invasion by variety of organisms (bacterial, viral, fungal or parasitic), with Staphylococcus aureus as the most common cause of infectious folliculitis.

Patients with superficial folliculitis present with multiple small folliculocentric erythematous papules and pustules, whereas deep folliculitis presents as a solitary tender abcess center on a hair follicle which is referred to as a furuncle (boil). Coalescence of adjacent furuncles often associated multiple sites of drainage is referred to as a carbuncle.  [1]  The type of inflammatory cells varies depending on the etiology of the folliculitis and/or the stage at which the biopsy specimen was obtained. [2, 3]

Histologically, in superficial folliculitis the inflammatory cells are restricted to follicular ostia and infundibulum, whereas the inflammation extends throughout the length of follicle and into surrounding dermis in cases of deep folliculitis. Deep folliculitis can be caused or exacerbated by manipulation of superficial folliculitis and potentially can eventuate in scaring.   The type of inflammatory cell varies depending upon the etiology of the folliculitis and/or stage of biopsy.

Perifolliculitis, on the other hand, is defined as the presence of inflammatory cells, usually lymphocytes, within the perifollicular tissues with focal extension into the adjacent reticular dermis. Folliculitis and perifolliculitis can occur independently or together as a result of follicular disruption and irritation.

When folliculitis is suspected, clinical history along with morphology and distribution of the lesions play an essential role in narrowing the differential diagnosis, but occasionally a gram stain, KOH or biopsy may be required to determine exact etiology. Management depends on extent of involvement, duration and underlying etiology.

 

Pathophysiology

Folliculitis refers to inflammation of the hair follicle and is classificed based upon which anatomic level of the hair follicle (superficial or deep) is involved; however, this distinction is not always clear cut. Folliculitis can also be subdivided into infective (bacterial, viral, fungal, or parasitic) and non-infectious etiologies with the latter most commonly arising due to follicular trauma, inflammation, occlusion or drug induced.

Eosinophilic folliculitis is a subtype of non-infectious folliculitides hypothesized to occur as a result of an autoimmune process directed against the sebocytes or some component of the sebum. [4, 5, 6]  Eosinophilic folliculitis has been classified as an AIDS-defining illness. [4, 5, 6]  In both children and adults, eosinophilic pustular folliculitis should be viewed as a possible cutaneous sign of immunosuppression. [7, 8] However, eosinophilic folliculitis may also develop in immunocompetent persons.

Although classically acne was classified as a follicular occlusive disorder, recently there has been a paradigm shift, and it is now felt to represent a primary inflammatory disorder of the pilosebaceous unit given that perifollicular inflammatory cells can be seen in the earliest stages of development prior to the appearance of the microcomedone. Hyperkeratinization then results in follicular obstruction, which allows for sebum accumulation resulting in further distension of the follicle. The normally commensal bacteria (Cutibacterium acnes formerly Propionibacterium acnes) forms a biofilm and its lipases break down sebum triglycerides into proinflammatory fatty acids and activate the innate immune response through toll-like receptor-2. [9, 10, 11]

Acne-related Medscape articles include Acne ConglobataAcne FulminansAcne Keloidalis NuchaeAcne Vulgaris, and Acneiform Eruptions.

Pseudofolliculitis barbae is another form of non-infectious folliculitis due to a local inflammatory reaction to ingrown hairs which penetrate the interfollicular skin. [12]

Papulopustular eruptions secondary to protein kinase inhibitors (epidermal growth factor receptor inhibitors) and various targeted therapies to treat advanced melanoma (BRAF, MEK  and immune checkpoint inhibitors) are hypothesized to occurs due to abnormal follicular epidermal differentiation which eventuates in follicular obstruction and subsequent inflammation. [13, 14, 15, 16]

Actinic folliculitis is rare form of non-infectious folliculitis of unclear etiology. In patients predisposed to this condition, UVA triggers an inflammtory response to thehair follicle due to an immune response and/or irritation which subsequently results in occulsion of the hair follicle. [17, 18]

Etiology

The most common causes of folliculitis include:

A. Infectious: bacterial, fungal, viral, parasitic, and folliculitis of secondary syphilis

B. Non-infectious: Friction (acne mechanica), Occlusion, Drug induced, Inflammatory

C. Idiopathic.

Predisposing factors include:

  • Altered immune status [4]
  • Prior skin injury  [19]
  • Friction (acne mechanica) and other causes of minor follicular trauma (plucking, shaving, waxing, electrolysis, laser) [20, 21]
  • Staphylococcal carrier status
  • Malnutrition
  • Diabetes
  • Obesity
  • Occlusion with topical products (paraffin or petrolum-based ointments, oils, grease, adhesive plasters)
  • Use of certain medications (topical and systemic steroids, lithium, phenytoin, disulfiram,  contraceptive agents, testosterone, danazol, stanozolol, antiepileptics, ethionamide, isoniazid, rifampicin, cyclosporin, sirolimus, epidermal growth factor receptor inhibitors, various targeted therapies to treat advanced melanoma, halogens (iodides and bromides), long-term use of antibiotics and occassionally excess vitamins (B1, B6, B12) [13, 14, 15, 16, 22, 23, 24, 25]
  • Folliculitis has also been reported following smallpox or anthrax vaccine. These cases are more common in military troops who are vaccinated prior to being deployed. [26]
  • Poorly chlorinated hot tubs [27]
  • Actinic damage [28]

Epidemiology

Frequency

Although superficial folliculitis is realtively common because it is often self-limited the exact incidence is unknown. Patients who present to thier primary care providers or to a dermatologist, typically have either recurrent or persistent superficial folliculitis or deep folliculitis.  Conditions that tend make patients more susceptible include shaving, immunosuppression, preexisting dermatoses, occlusive clothing, and/or occuslsive topical products, exposure to hot humid temperatures, diabetes mellitus, obesity, long-term use of antibiotics and use of other medications.

The acneiform eruption attributed to epidermal growth factor receptor inhibitors occurs in 50-100% of patients and is a dose-dependent drug reaction. [13, 14, 15, 16]

Race

Folliculitis occurs in persons of any race, but pseudofolliculitis and traction folliculitis more frequently occurs in African Americans, whereas classic eosinophilic folliculitis is more common in persons of Japanese origin. [6, 20, 29, 12]

Sex

Although most cases of folliculitis show no sex predilection, folliculitis barbae, folliculitis keloidalis nuchae, perifolliculitis capitis abscedens et suffodiens, and eosinophilic folliculitis occurs more frequently in males, whereas traction folliculitis occurs more frequently in females. [6, 20, 29, 10, 12, 30]

Age

Folliculitis can be seen in persons of all ages; however, Malassezia (Pityrosporum) folliculitis tends to occur more often in adolescents, presumably because of the increased activity of their sebaceous glands. [31, 32]

Patient Education

Most cases will resolve on own but antimicrobial cleansers, benzoyl peroxide acne wash or salicylic acne wash may hasten improvement.  Recommend avoidance of shaving, wearing tight fitting clothing, and use of occlusive skin products. Patients should avoid repetitive touching of the skin, sharing towels and implement good handwashing practices.  Ensure hot-tubs are well-maintained and properly chlorinated, wash bathing suit or wet suit after each use and let dry before re-wearing.  

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