> Table of Contents > Folliculitis
David L. Anderson, MD
Thomas P. Garigan, MD, MA
image BASICS
  • Superficial inflammation of a follicle, usually a hair follicle, caused by infection, local trauma, or chemical irritation (1)
  • Can occur anywhere on the body that hair is found
  • Most frequent symptom is pruritus.
  • Painless or tender pustules, vesicles, or pink/red papulopustules up to 5 mm in size.
  • Most commonly infectious in etiology:
    • Staphylococcus aureus bacteria (most common)
    • Pseudomonas aeruginosa infects areas of the body exposed to poorly chlorinated hot tubs, pools, or contaminated water.
    • Aeromonas hydrophila with recreational water exposure
    • Fungal (dermatophytic, Pityrosporum, Candida)
    • Viral (VZV, herpes simplex virus [HSV])
    • Parasitic (Demodex spp. mites, schistosomes)
  • Noninfectious types
    • Acneiform folliculitis
    • Actinic superficial folliculitis
    • Acne vulgaris
    • Keloidal folliculitis
    • Folliculitis decalvans
    • Perioral dermatitis
    • Rosacea
    • Fox-Fordyce disease
    • Pruritus folliculitis of pregnancy
    • Eosinophilic pustular folliculitis (three variants: Ofuji disease in patients of Asian descent, HIV-positive/immunocompromised, infantile)
    • Toxic erythema of the newborn
    • Eosinophilic folliculitis (seen in HIV-positive/immunocompromised)
    • Follicular mucinosis
  • Skin disorders may produce a follicular eruption that includes the following:
    • Pseudofolliculitis: similar in appearance; occurs after shaving; affects the face, scalp, pubis, and legs. Pseudofolliculitis barbae, or razor bumps, occurs frequently in black men.
    • Atopic dermatitis
    • Follicular psoriasis
Affects persons of all ages, gender, and race
Predisposing factors to folliculitis
  • Chronic staphylococcal carrier
  • Diabetes mellitus
  • Malnutrition
  • Pruritic skin disease (e.g., scabies, eczema, etc.)
  • Exposure to poorly chlorinated swimming pools/hot tubs or water contaminated with P. aeruginosa, A. hydrophila, or schistosomes
  • Occlusive corticosteroid use (for multiple hours)
  • Bacteria
    • Superficial or deep
    • Most frequently due to S. aureus (increasing number of MRSA cases)
    • Also due to Streptococcus species, Pseudomonas (following exposure to water contaminated with the species), or Proteus.
    • May progress to furunculosis (painful pustular nodule with central necrosis that leaves a permanent scar after healing)
  • Fungal
    • Dermatophytic (tinea capitis, corporis, pedis)
    • Pityrosporum (Pityrosporum orbiculare) commonly affecting teenagers and men, predominantly on upper chest and back
    • Candida albicans, although rare, has been reported with broad spectrum antibiotic use, glucocorticoid use, immunosuppression, and in those who abuse heroin, resulting in candidemia that leads to pustules and nodules in hair-bearing areas.
  • Viral
    • HSV
    • May be due to molluscum contagiosum, usually a sign of immunosuppression
  • Parasitic
    • Demodex spp. mites (most commonly Demodex folliculorum)
    • Schistosomes (swimmer's itch)
  • Acneiform type commonly drug-induced (systemic and topical corticosteroids, lithium, isoniazid, rifampin), EGFR inhibitors
  • Severe vitamin C deficiency
  • Actinic superficial type occurs within 24 to 48 hours of exposure to the sun, resulting in multiple follicular pustules on the shoulders, trunk, and arms.
  • Acne vulgaris
  • Keloidal folliculitis is a chronic condition affecting mostly black patients; involves the neck and occipital scalp, resulting in hypertrophic scars and hair loss; usually secondary to folliculitis barbae from shaving
  • Folliculitis decalvans is a chronic folliculitis that leads to progressive scarring and alopecia of the scalp.
  • Rosacea consists of papules, pustules, and/or telangiectasias of the face; individuals are genetically predisposed. Helicobacter pylori and D. folliculorum have also been implicated.
  • Perioral dermatitis seen most commonly in children and young women; restricted to the perioral region as well as the lower eyelids. May be due to cosmetics, hyperandrogenemia, or use of fluorinated topical corticosteroids
    • Typically spares vermillion border
  • Fox-Fordyce disease affects the skin containing apocrine sweat glands (i.e., axillae), resulting in chronic pruritic, annular, follicular papules.
  • Eosinophilic pustular folliculitis (EPF) has three variants: classic (Ofuji disease), associated with HIV infection, and infantile
  • Toxic erythema of the newborn is a self-limiting pustular eruption usually appearing during the first 3 to 4 days of life and subsequently fading in the following 2 weeks.
  • Malassezia infections in adult males with lesions on trunk (2)
  • Hair removal (shaving, plucking, waxing, epilating agents)
  • Other pruritic skin conditions: eczema, scabies
  • Occlusive dressing or clothing
  • Personal carrier or contact with methicillin-resistant S. aureus (MRSA)-infected persons
  • Diabetes mellitus
  • Immunosuppression (medications, chemotherapy, HIV)
  • Use of hot tubs or saunas
  • Use of EGFR inhibitors
  • Chronic antibiotic use (gram-negative folliculitis)
  • Good hygiene practices
    • Wash hands frequently.
    • Antimicrobial soap
    • Wash towels, clothes, and linens frequently with hot water to avoid reinfection.
  • Good hair removal practices
    • Exfoliate beforehand.
    • Use witch hazel, alcohol, or Tend Skin afterward.
    • Shave in direction of hair growth; use moisturizer/warm water.
    • Decrease frequency of shaving
    • Use clippers primarily or single-blade razors if straight shaving is desired.
  • Impetigo
  • Furunculosis
  • Scabies
  • Acne
  • Follicular psoriasis
  • Eczema
  • Characteristic lesions are 1- to 5-mm-wide vesicles, pustules, or papulopustules with surrounding erythema.
  • Rash occurs on hair-bearing skin, especially the face (beard), proximal limbs, scalp, and pubis.
  • Pseudomonal folliculitis appears as a widespread rash, mainly on the trunk and limbs.
  • In pseudofolliculitis, the growing hair curls around and penetrates the skin at shaved areas.
  • Acne vulgaris/acneiform eruptions
  • Arthropod bite
  • Contact dermatitis
  • Cutaneous candidiasis
  • Milia
  • Atopic dermatitis
  • Follicular psoriasis
  • Hidradenitis suppurativa
Initial Tests (lab, imaging)
  • Diagnosis is usually made clinically, taking risk factors, history, and location of lesion into account.
  • Culture and Gram stain of the pustule by scraping the pustule with a no. 15 blade and not directly swabbing the skin to identify infectious agent and sensitivities to antibiotics
  • P.383

  • KOH preparation as well as Wood lamp fluorescence to identify Candida or yeast
  • Tzanck smear where suspicion of herpetic simplex viral folliculitis is high
Follow-Up Tests & Special Considerations
  • If risk factors or clinical suspicion exist, consider serologies for HIV or syphilis.
  • If recurrent, consider HIV testing and A1C/fasting blood sugar testing to evaluate for diabetes.
  • Punch biopsy may be considered if lesions persist despite treatment (3)[C].
Test Interpretation
  • Treat positive bacterial culture according to sensitivities.
  • Positive HIV serology: Follow up with CD4 count and punch biopsy to rule out eosinophilic folliculitis.
  • Eosinophilic folliculitis: Collect eosinophils within superficial follicle (4).
  • Lesions usually resolve spontaneously.
  • Avoid shaving and waxing affected areas (5)[C].
  • Warm compresses may be applied TID.
  • Systemic antibiotics are typically unnecessary.
  • Topical mupirocin may be used in presumed S. aureus infection.
  • Topical antifungals for fungal folliculitis (2)[B]
  • Preventive measures are keys to avoidance of recurrence:
    • Antibacterial soaps (Dial soap, chlorhexidine, or benzyl peroxide wash when showering/bathing)
    • Bleach baths (1/2 cup of 6% bleach per standard bathtub, and soak for 5 to 15 minutes followed by water rinse 1 to 2 times a week)
    • Keep skin intact; daily skin care with noncomedogenic moisturizers; avoid scratching.
    • Clean shaving instruments daily or use disposable razor, disposing after 1 use.
    • Change washcloths, towels, and sheets daily.
Antiseptic and supportive care is usually enough. Systemic antibiotics may be used with questionable efficacy.
First Line
  • Staphylococcal folliculitis
    • Mupirocin ointment applied TID for 10 days
    • Cephalosporin (cephalexin): 250 to 500 mg PO QID for 7 to 10 days
    • Dicloxacillin: 250 to 500 mg PO QID for 7 to 10 days
  • For MRSA
    • Bactrim DS: 1 to 2 tablets (160 mg/800 mg) BID PO for 5 to 10 days
    • Clindamycin: 300 mg PO TID for 10 to 14 days
    • Minocycline: 200 mg PO initially then 100 mg BID for 5 to 10 days
    • Doxycycline: 50 to 100 mg PO BID for 5 to 10 days
  • Pseudomonal folliculitis
    • Topical dilute acetic acid baths
    • Ciprofloxacin: 500 to 750 mg PO BID for 7 to 14 days only if patient is immunocompromised or lesions are persistent
  • Eosinophilic folliculitis/eosinophilic pustular folliculitis
    • HAART treatment for HIV-positive-related causes
    • Topical corticosteroids: betamethasone 0.1% BID for 3 to 24 weeks or
    • Antihistamines (hydroxyzine, cetirizine) or
    • Tacrolimus topically BID for 3 to 24 weeks or
    • Isotretinoin 0.5 mg/kg/day PO for 4 to 8 weeks or
    • Itraconazole or metronidazole
  • Fungal folliculitis
    • Topical antifungals: ketoconazole 2% cream or shampoo or selenium sulfide shampoo daily or
    • Econazole cream applied to affected area BID for 2 to 3 weeks
      • Systemic antifungals for relapses fluconazole (100 to 200 mg/day for 3 weeks) or itraconazole (200 mg/day for 1 to 3 weeks)
      • Griseofulvin (tinea capitis in children; 10 to 20 mg/kg/day for 6 weeks minimum)
  • Parasitic folliculitis
    • 5% permethrin: Apply to affected area, leave on for 8 hours, and wash off.
    • Ivermectin: 200 &mgr;g/kg × 1 followed by topical permethrin
  • Herpetic folliculitis
    • Valacyclovir: 500 mg PO TID for 5 to 10 days or
    • Famciclovir: 500 mg PO TID for 5 to 10 days or
    • Acyclovir: 200 mg PO 5 times daily for 5 to 10 days
Unusual or persistent cases should be biopsied and then referred to dermatology.
Public Health Measures
  • Outbreaks of culture-positive Pseudomonas hot tub folliculitis should be reported so that source identification can be determined and superchlorination (14 parts/million) can occur.
Incision and drainage is unlikely to be necessary and typically not preferred due to potential for scar formation.
Patient Monitoring
  • Resistant cases should be followed every 2 weeks until cleared.
  • One return visit in 2 weeks if symptoms abate
For obese patients, weight reduction will decrease skin-on-skin friction.
Avoid shaving in involved areas.
  • Usually resolves with treatment; however, S. aureus carriers may experience recurrences.
  • Mupirocin nasal treatment for carrier status and for family/household members might be helpful.
  • Resistant or severe cases may warrant testing for diabetes mellitus or immunodeficiency (HIV) (3)[C].
1. Breitkopf T, Leung G, Yu M, et al. The basic science of hair biology: what are the causal mechanisms for the disordered hair follicle? Dermatol Clin. 2013;31(1):1-19.
2. Song HS, Kim SK, Kim YC. Comparison between Malassezia folliculitis and non-Malassezia folliculitis. Ann Dermatol. 2014;26(5):598-602.
3. Tilley DH, Satter EK, Kakimoto CV, et al. Disseminated verrucous varicella zoster with exclusive follicular involvement. Arch Dermatol. 2012;148(3):405-407.
4. Annam V, Yelikar BR, Inamadar AC, et al. Clinicopatholigical study of itchy folliculitis in HIV-infected patients. Indian J Dermatol Venereol Leprol. 2010;76(3):259-262.
5. Khanna N, Chandramohan K, Khaitan BK, et al. Post waxing folliculitis: a clinicopathological evaluation. Int J Dermatol. 2014;53(7):849-854.
Additional Reading
  • Bachet JB, Peuvrel L, Bachmeyer C, et al. Folliculitis induced by EGFR inhibitors, preventive and curative efficacy of tetracyclines in the management and incidence rates according to the type of EGFR inhibitor administered: a systematic literature review. Oncologist. 2012;17(4):555-568.
  • Böer A, Herder N, Winter K, et al. Herpes folliculitis: clinical, histopathological, and molecular pathologic observations. Br J Dermatol. 2006;154(4):743-746.
  • Brooke RCC, Griffiths CEM. Folliculitis decalvans. Clin Exp Dermatol. 2001;26(1):120-122.
  • Ellis E, Scheinfeld N. Eosinophilic pustular folliculitis: a comprehensive review of treatment options. Am J Clin Dermatol. 2004;5(3):189-197.
  • Fiorillo L, Zucker M, Sawyer D, et al. The Pseudomonas hot-foot syndrome. N Engl J Med. 2001;345(5): 335-338.
  • Fridkin SK, Hageman JC, Morrison M, et al. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med. 2005;352(14):1436-1444.
  • James WD. Clinical practice. Acne. N Engl J Med. 2005;352(14):1463-1472.
  • Luelmo-Aguilar J, Santandreu MS. Folliculitis: recognition and management. Am J Clin Dermatol. 2004;5(5):301-310.
  • Nervi SJ, Schwartz RA, Dmochowski M. Eosinophilic pustular folliculitis: a 40 year retrospect. J Am Acad Dermatol. 2006;55(2):285-289.
See Also
Algorithm: Rash, Focal
  • L73.9 Follicular disorder, unspecified
  • L66.2 Folliculitis decalvans
  • L73.8 Other specified follicular disorders
Clinical Pearls
  • Folliculitis lesions are typically 1 to 5 mm clusters of pruritic erythematous papules and pustules.
  • Most commonly due to S. aureus. If community has increased incidence of MRSA, consider anti-MRSA treatment.
  • It is extremely important to educate patients on proper hygiene and skin care techniques in order to prevent chronic or recurrent cases.