Infectious folliculitis
BACTERIAL FOLLICULITIS — Bacterial infection is the most common cause of infectious folliculitis.
Etiology and risk factors —
●Staphylococcus aureus – a gram-+ bacterium. The most common cause.
= "Impetigo of Bockhart"
Both methicillin-sensitive and methicillin-resistant S. aureus (MRSA) can cause folliculitis.
●Gram-negative folliculitis – Pseudomonas aeruginosa, cause of "hot tub folliculitis," a form of folliculitis attributed to contact with water contaminated with Pseudomonas as a result of inadequate chlorine, bromine, or pH levels in whirlpools, hot tubs, or swimming pools [2]. Bathing with contaminated sponges or nylon towels and use of contaminated rubber gloves are additional potential modes of acquisition [3-5].
Klebsiella, Enterobacter, and Proteusspecies: associated with long-term treatment with oral antibiotics (eg, tetracyclines) for acne vulgaris [6].
Aeromonas hydrophila: after recreational water exposure.
Factors that may increase risk include [8]:
●Nasal carriage of S. aureus
●Occlusion of hair follicles
●Hyperhidrosis
●Underlying pruritic skin disease (eg, atopic dermatitis)
●Prolonged application of topical corticosteroids
●Long-term oral antibiotic therapy for acne
●Shaving against the direction of hair growth
●Exposure to hot tubs or heated swimming pools
●Male sex (for gram-negative folliculitis associated with oral antibiotic therapy for acne vulgaris) [6]
Clinical manifestations —
Follicular pustules and follicular erythematous papules (picture 1A-D). Pruritus is common or painful pustules.
Can occur on any hair-bearing area: ++on the scalp and face [9], upper trunk, buttocks, and legs, as well as the axillae in infants and children [8]. Community-acquired MRSA folliculitis may be more likely to occur on the chest, flanks, scrotum, and periumbilical region than methicillin-sensitive S. aureus infections [1].
Folliculitis barbae : tender pustules within erythematous plaques involving multiple hair follicles [8,9].
"Hot tub folliculitis" : pruritic follicular macules, papules, or pustules (picture 2A-B). The eruption appears 8 to 48 hours after exposure and primarily occurs on the trunk and buttocks in the distribution of the wet bathing suit or other areas exposed to contaminated water.
Klebsiella, Enterobacter, or Proteu: typically occurs on the face, most commonly in the perinasal region.
Diagnosis — Bacterial folliculitis is usually diagnosed by means of the patient history and physical examination
Further work-up is primarily reserved for patients with an unclear diagnosis or treatment-resistant disease. A Gram stain and culture of the contents of a pustule can confirm the presence of infection and identify the causative organism. Infrequently, a skin biopsy is necessary to differentiate folliculitis from other skin conditions. Histopathologic examination of bacterial folliculitis shows neutrophils infiltrating a hair follicle (picture 3) [9].
Differential diagnosis —
Face
●Acne vulgaris – The characteristic clinical features of acne vulgaris are open and closed comedones and inflammatory papules and pustules on the face, chest, shoulders, or back (picture 4). The presence of comedones and a lack of pruritus are more consistent with acne vulgaris than folliculitis.
●Papulopustular rosacea – primarily affects adults and presents with pustules and erythematous papules on the central face (picture 5). Exacerbating factors such as alcohol, spicy foods, sun exposure, and temperature changes are common.
●Perioral (periorificial) dermatitis – Perioral dermatitis presents with small erythematous papules around the mouth, nose, or periorbital areas (picture 6). There may be associated mild scale. Most common in young women.
●Acne keloidalis nuchae – Acne keloidalis nuchae is a chronic, scarring folliculitis that primarily affects males of African descent. Papules, pustules, and keloid-like papules and plaques develop on the posterior scalp (picture 7).
Frunk or extremities:
●Drug-induced folliculitis – A monomorphic papulopustular eruption on the trunk and arms known as "steroid folliculitis" or "steroid acne" may occur after administration of systemic glucocorticoids (picture 9A-B) [11]. Other drugs that may cause folliculitis-like eruptions include phenytoin, lithium, isoniazid,cyclosporine, halogens, and epidermal growth factor receptor inhibitors (picture 10).
●Keratosis pilaris – Keratosis pilaris is a common disorder of follicular keratinization that presents with asymptomatic, keratotic follicular papules on the upper arms, face, thighs, and buttocks (picture 11). Keratosis pilaris is most commonly seen in children and young adults.
●Hidradenitis suppurativa – Hidradenitis suppurativa is a chronic inflammatory skin disorder characterized by the development of inflamed nodules, abscesses, and sinus tracts (picture 12). Involvement occurs primarily in the axillary, mammary, and inguinal areas.
●Scabies – Sarcoptes scabiei infestation often presents with intensely pruritic pustules and papules in the axillae, inguinal areas, interdigital web spaces, waistline, and volar wrists (picture 13).
●Grover's disease (transient acantholytic dermatosis) – Grover's disease most commonly presents as erythematous papules on the chest and back in men in their fifth decade or older (picture 14). Histopathology demonstrates focal acantholytic dyskeratosis that is not centered upon hair follicles.
Treatment —
Staphylococcal folliculitis — Treatment of staphylococcal folliculitis is not always necessary; mild folliculitis with few pustules often resolves spontaneously. Patients with numerous papules or pustules or with involvement of more than one body area are good candidates for medical treatment. Folliculitis that does not resolve spontaneously after several weeks also should be treated.
●Medical therapy –
Topical antibiotic : First-line agents are topical mupirocin and topical clindamycin [12].
Topical fusidic acid is an additional first-line treatment option; however, increasing resistance of S. aureus to fusidic acid has been observed in areas where fusidic acid use is common.
Topical erythromycin may also be effective; however, topical erythromycin has fallen out of favor as a first-line treatment in many locations due to increasing prevalence of erythromycin-resistance and community-acquired MRSA infections [1].
Oral antibiotherapy:. A 7- to 10-day course is usually sufficient.
Beta-lactam antibiotics such as dicloxacillin (250 to 500 mg four times per day) and cephalexin (250 to 500 mg four times per day) are first-line systemic treatments [9,14].
If MRSA is cultured or suspected, the patient should be treated with a 7- to 10-day course of oral trimethoprim/sulfamethoxazole (1 to 2 DS tablets twice daily), clindamycin (300 to 450 mg four times per day), or doxycycline (100 mg twice daily).
●Prevention –
Avoidance of predisposing factors for folliculitis (eg, occlusive clothing, hyperhidrosis).
A decolonization regimen, such as a five-day course of topical mupirocin ointment in the nares and daily chlorhexidine body washes + daily decontamination of personal items (eg, towels, clothing) has been suggested for patients with recurrent abscesses in an attempt to reduce recurrences [16].
Gram-negative folliculitis — resolves within 7 to 10 days with just good skin hygiene. Avoidance of risk factors. Oral ciprofloxacin (250 to 750 mg twice daily) can be used for severe cases or immunocompromised patients [8].
Selection of an antibiotic for gram-negative folliculitis due to long-term systemic antibiotic therapy should be guided by testing to determine antibiotic sensitivity of the causative organism. Ampicillin (250 to 500 mg four times daily), trimethoprim/sulfamethoxazole (1 DS tablet twice daily), or ciprofloxacin (250 to 750 mg twice daily) are common first-line treatments. Treatment with these agents is for an additional 14 days after clinical resolution [9]. Oral isotretinoin (0.5 to 1 mg/kg daily for four to five months) is the treatment of choice for recalcitrant disease [17].
FUNGAL FOLLICULITIS — After S. aureus, fungi are the most commonly detected microorganisms in folliculitis.
Etiology and risk factors —
●Malassezia (Pityrosporum) folliculitis – Multiple species of Malassezia, lipophilic yeasts present in the normal cutaneous flora, cause folliculitis.
Malassezia folliculitis is more common in males than in females. It is also most likely to occur in adolescents and among individuals in hot, humid climates. High sebum production in adolescents and increased sweating are both predisposing factors for Malassezia folliculitis [19]. Other predisposing factors include topical or oral antibiotic use and immunosuppression [21-23].
●Dermatophyte folliculitis – Trichophyton, Epidermophyton, and Microsporum species are the usual causes of dermatophyte folliculitis. Tinea capitis (dermatophyte infection of the scalp) and tinea barbae (dermatophyte infection of the beard or mustache areas). Dermatophyte folliculitis can also occur as a secondary feature of tinea corporis, tinea cruris, and tinea pedis. (See "Dermatophyte (tinea) infections".)
Majocchi's granuloma is a clinical subtype of dermatophyte folliculitis occurring on sites other than the scalp and beard. Majocchi's granuloma is characterized by deep follicular and dermal involvement and is commonly caused by T. rubrum [8]. Predisposing factors include shaving of the legs, topical corticosteroid use, and immunocompromised status [24].
●Candida folliculitis –
Clinical manifestations —
Malassezia folliculitis : pruritic, monomorphic, follicular papules or pustules on the face, back, extensor side of arms, chest, and neck (picture 15A-B). The central face is usually spared with involvement of the forehead, chin, and sides of the face [19].
Dermatophyte folliculitis often manifests as follicular pustules surrounded by an erythematous plaque (picture 16A-D). Associated features vary depending on the location of the infection. The most common presentation of Majocchi's granuloma is a unilateral eruption on the lower extremity (picture 16C-D). The upper extremities, specifically the forearm and dorsal hand, are additional common locations. Hair loss is common and the inflammation can be suppurative and granulomatous, depending on the depth of infection [8]. (See"Dermatophyte (tinea) infections", section on 'Majocchi's granuloma'.)
Candida folliculitis has been described as a widely distributed pustular folliculitis [8]. In rare cases, Candidafolliculitis mimics tinea barbae, manifesting as a fluctuant plaque on the face with follicular pustules and papules [25].
Diagnosis — To confirm fungal folliculitis, a potassium hydroxide (KOH) examination can be performed on skin scrapings from an involved area. Hyphae suggest a dermatophyte folliculitis (picture 17) [24], whereas yeast cells and pseudohyphae suggest Candida infection (picture 18) [25]. Budding spores and short, curved hyphae are suggestive of Malassezia species. (See "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep'.)
Although a standard KOH preparation is usually sufficient, a commercial or compounded KOH solution mixed with ink can facilitate visualization of hyphae and spores. In addition, a study that included 49 patients withMalassezia follicultis found that staining skin scrapings with a May-Grünwald-Giemsa stain was more effective than a KOH preparation in detecting Malassezia [19].
Differential diagnosis — see above
Treatment — The approach to the treatment of fungal folliculitis depends on the etiology. Oral antifungal agents such as fluconazole and itraconazole are common treatments. Oral ketoconazole should not be used for the treatment of any form of fungal folliculitis due to risks of liver injury, adrenal gland disorders, and significant drug interactions [27].
●Malassezia folliculitis – Systemic antifungal therapy may be more effective than topical treatments [27].
oral fluconazole 100 to 200 mg daily for one to four weeks or 300 mg once weekly for one to two months [27].
Recurrence is common after treatment. Long-term periodic (eg, once- or twice-weekly) use of topical treatments, often selenium sulfide, ketoconazole, or ciclopirox shampoos, is often performed in an attempt to prevent recurrence of disease [30].
●Dermatophyte folliculitis – tinea barbae in adults with a two- to four-week course of griseofulvin microsize (500 mg per day) or oral terbinafine (250 mg per day). Itraconazoleand fluconazole are also effective for dermatophyte folliculitis [8,24].
●Candida folliculitis – systemic itraconazole or fluconazole.
VIRAL FOLLICULITIS —
Etiology and risk factors — Herpes folliculitis is a rare manifestation of herpesvirus infections. It is most commonly associated with varicella zoster virus (VZV) infection
Molluscum contagiosum virus (MCV) is a poxvirus that preferentially affects children and immunocompromised adults, but also occurs in healthy adults.
Clinical manifestations — Erythematous papules, pustules, vesicles, papulovesicles, and [33,37]. These lesions are often grouped or clustered [37]. HSV folliculitis in the beard area (herpetic sycosis) is reported most commonly in immunocompromised patients, but may also occur in the absence of immunosuppression [38,39].
Papules and pustules along with characteristic umbilicated papules are typical findings in molluscum folliculitis. Presentations resembling tinea barbae and pseudolymphoma have been reported [34,38,39].
Diagnosis — Viral culture, polymerase chain reaction (PCR), or immunofluorescence testing should be performed to confirm the diagnosis if herpes folliculitis is suspected [37].
MCV , where the diagnosis is unclear, a skin biopsy will reveal characteristic molluscum bodies (Henderson-Patterson bodies) in the follicular epithelium [34].
Treatment — Herpes folliculitis can be treated with 5 to 10 days of oral acyclovir (200 mg five times per day),valacyclovir (500 mg three times per day), or famciclovir (500 mg three times per day).
Molluscum folliculitis : curettage, cantharidin, and cryotherapy. Podophyllotoxin and trichloroacetic acid are additional treatments [8].
DEMODEX FOLLICULITIS — Demodex folliculorum is a mite belonging to the class of arachnids and a proposed cause of facial folliculitis. Demodex mites are also proposed to contribute to the pathogenesis of papulopustular rosacea and chronic blepharitis [11,40].
Etiology and risk factors — The role of D. folliculorum in folliculitis is controversial because the mite is a common inhabitant of the pilosebaceous unit in normal skin. Up to 80 to 90 percent of humans may harbor theDemodex organism [41]. Support for a pathogenic role in folliculitis and rosacea stems from improvement in these disorders with anti-Demodex therapies [8]. In addition, increased density of mites in the skin has been detected in patients with rosacea [42].
Demodex folliculitis is most frequently diagnosed in adults. However, Demodex folliculitis also has been implicated in facial pustules and papules in children [43]. Immunosuppression may increase risk for cutaneous manifestations of Demodex infection [44].
Clinical manifestations — Demodex folliculitis is usually characterized by rosacea-like inflammatory papules and pustules on the face [41]. In addition, authors have described nodulocystic and conglobate (abscess-like) presentations [45].
Diagnosis — Demodex folliculitis is often first suspected when patients with a rosacea-like papulopustular eruption fail to respond to antibiotic therapy for rosacea. A potassium hydroxide (KOH) preparation of a skin scraping from an involved area is typically used to detect Demodex mites. Clinical correlation is necessary for the interpretation of the KOH preparation because Demodex mites can be detected in normal skin and a definitive threshold for diagnosis has not been established. In general, the KOH preparation may be considered positive when more than a few mites are detected [41]. Although not typically performed in clinical practice, more than five mites per cm2 detected on an adhesive skin-surface biopsy utilizing a cyanoacrylic adhesive has been proposed as a threshold for use in clinical studies [46].
Demodex mites may also be detected on skin biopsy. As with a KOH preparation, visualization of Demodex is not sufficient to confirm the diagnosis in the absence of clinical correlation because Demodex mites can be present in follicles in normal skin.
Differential diagnosis — The differential diagnosis for Demodex folliculitis is similar to the differential diagnosis of facial bacterial folliculitis. (See 'Differential diagnosis' above.)
Treatment — Data on treatment options for Demodex folliculitis are limited. Topical permethrin 5% cream, topical sulfur, oral ivermectin, and oral metronidazole are reasonable treatments [42]. The findings of one randomized trial suggest that combination therapy with oral ivermectin and oral metronidazole is more effective for reducing mite counts than oral ivermectin monotherapy [40]; however, further study is necessary to confirm whether combination therapy is indicated for Demodex folliculitis. The efficacy of topical ivermectin remains to be determined.
We typically treat with permethrin 5% cream or oral ivermectin. Topical permethrin can be applied to the entire face before bed and washed off after 8 to 14 hours. Oral ivermectin can be given as two 200 mcg/kg doses separated by one week.