Infectious folliculitis

INTRODUCTION — Folliculitis refers to inflammation of the superficial or deep portion of the hair follicle. The classic clinical findings of superficial folliculitis are folliculocentric, inflamed papules and/or pustules on hair-bearing skin (picture 1A-C). Nodules are a feature of deep, follicular inflammation.

Folliculitis may be infectious or, less frequently, noninfectious. Various bacteria, fungi, viruses, and parasites are causes of infectious folliculitis, with bacteria as the most common cause.

A correct diagnosis of infectious folliculitis is essential for appropriate management. The patient history and physical examination, particularly the assessment of the distribution of folliculitis, help to narrow the differential diagnosis. Detection of the causative organism confirms the diagnosis and may help direct therapy. (See 'Diagnosis' below.)

The etiologies, clinical manifestations, diagnosis, and management of infectious folliculitis will be reviewed here. Noninfectious causes of folliculitis are reviewed separately.

●(See "Approach to the patient with pustular skin lesions".)

●(See "Approach to the patient with a scalp disorder", section on 'Pustules'.)

●(See "HIV-associated eosinophilic folliculitis".)

●(See "Folliculitis decalvans".)

●(See "Perforating dermatoses", section on 'Perforating folliculitis'.)

MAJOR SUBTYPES — The major subtypes of infectious folliculitis include bacterial, fungal, viral, and parasitic folliculitis. The most commonly reported clinical variants of these subtypes are as follows:

●Bacterial:

•Staphylococcal folliculitis

•Pseudomonal folliculitis

•Gram-negative folliculitis

●Fungal:

•Malassezia (Pityrosporum) folliculitis

•Dermatophytic folliculitis

•Candida (candidal) folliculitis

●Viral:

•Herpetic folliculitis

•Molluscum folliculitis (rare)

●Parasitic:

•Demodex (demodectic) folliculitis

WHEN TO SUSPECT — A diagnosis of infectious folliculitis should be considered in patients presenting with folliculocentric papules and pustules.

The physical examination and patient history play important roles in narrowing the differential diagnosis. Assessments of the distribution of involvement, associated clinical findings, and risk factors for folliculitis are particularly helpful for identifying features that suggest specific types of infectious folliculitis:

●Common distributions:

•Scalp – Staphylococcus aureus folliculitis or dermatophytic folliculitis (tinea capitis)

•Face – S. aureus, Demodex, or gram-negative folliculitis

•Beard – S. aureus folliculitis (sycosis barbae), dermatophytic folliculitis (tinea barbae), Candida folliculitis, or herpetic folliculitis (herpetic sycosis)

•Trunk or extremities – S. aureus, pseudomonal, Malassezia, dermatophytic, or Candida folliculitis

●Associated physical findings:

•Monomorphic, follicularly based papules, particularly on the posterior trunk – Malassezia folliculitis

•Grouped or clustered lesions – Herpetic folliculitis (varicella zoster virus [VZV] or herpes simplex virus [HSV])

•Umbilicated papules – Molluscum folliculitis

●Risk factors:

•Exposure to hot tubs or heated swimming pools – Pseudomonal folliculitis

•Prolonged oral antibiotic therapy – Gram-negative folliculitis

•Immunosuppression – Increases suspicion for fungal, viral, or demodectic folliculitis

The clinical assessment is also helpful for identifying patients with features supportive of other disorders. Examples of features that should prompt consideration of other disorders include:

●Lesions that are not centered around follicles

●Keratotic, follicular papules as the primary finding (suggests a disorder of follicular keratinization [eg, keratosis pilaris, lichen spinulosus, phrynoderma])

●Absence of any clinical signs of inflammation, such as erythema, hyperpigmentation, or tenderness

In addition, given the common presence of pustules in infectious folliculitis, an absence of pustules should raise suspicion for an alternative diagnosis but does not rule out infectious folliculitis.

Examples of common disorders in the differential diagnosis of infectious folliculitis are reviewed below. (See 'Differential diagnosis' below.)

ETIOLOGY AND CLINICAL FEATURES

Bacterial folliculitis — Bacterial infection is the most common cause of infectious folliculitis. Common causes of bacterial folliculitis include S. aureus and gram-negative bacteria. (See 'Staphylococcal folliculitis' below and 'Pseudomonal folliculitis' below and 'Other gram-negative folliculitis' below.)

Staphylococcal folliculitis

●Etiology and risk factors – S. aureus, a gram-positive bacterium, is the most common cause of bacterial folliculitis. "Impetigo of Bockhart" and "Bockhart impetigo" are alternative terms for superficial staphylococcal folliculitis.

Both methicillin-sensitive Staphylococcus aureus (MSSA) and methicillin-resistant Staphylococcus aureus (MRSA) can cause folliculitis. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology" and "Methicillin-resistant Staphylococcus aureus infections in children: Epidemiology and clinical spectrum".)

Coagulase-negative staphylococci species (Staphylococcus epidermidis and Staphylococcus capitis) have also been associated with bacterial folliculitis [1,2].

Staphylococcal folliculitis can occur in infants, children, or adults. Examples of factors that may increase risk include nasal carriage of S. aureus, hyperhidrosis, occlusion of hair follicles, and shaving [3].

●Clinical manifestations – The classic clinical findings in bacterial folliculitis are follicular pustules and inflamed, follicular papules (picture 1A-B, 1D-E). Common sites include the scalp, face, upper trunk, buttocks, and legs, as well as the axillae in infants and children [3,4]. Pruritus is common. Tender lesions may be present.

Folliculitis barbae (also known as sycosis barbae) is a bacterial folliculitis involving deep portions of the hair follicles in the beard areas of the face and neck. S. aureus is a frequent causative organism. Folliculitis barbae often presents with tender pustules within erythematous plaques involving multiple hair follicles (picture 2) [3,4].

Pseudomonal folliculitis

●Etiology and risk factors – Pseudomonas aeruginosa is a gram-negative bacterium and the 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 [5]. Bathing with contaminated sponges or nylon towels and use of contaminated rubber gloves are additional potential modes of acquisition [6-8]. (See "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Hot tub-associated eruptions'.)

●Clinical manifestations – "Hot tub folliculitis" induced by P. aeruginosa presents with pruritic, inflamed, follicular macules, papules, or pustules (picture 3A-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 [5]. (See "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Hot tub-associated eruptions'.)

Other gram-negative folliculitis

●Etiology and risk factors – Other organisms often responsible for gram-negative folliculitis include Klebsiella, Enterobacter, and Proteus species. In addition, Aeromonas hydrophila, another gram-negative organism, has been linked to folliculitis after exposure to water [9].

Gram-negative folliculitis has been associated with long-term treatment with oral antibiotics (eg, tetracyclines) for acne vulgaris or rosacea but may also occur in the absence of this history [10]. When gram-negative folliculitis occurs in association with long-term antibiotic therapy, it usually has an explosive onset. Male sex may be a risk factor; in one series, males accounted for 39 of 46 patients with gram-negative folliculitis [10]. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Gram-negative folliculitis'.)

●Clinical manifestations – Patients usually present with erythematous papules and pustules on the face, most commonly in the perinasal region. Proteus mirabilis gram negative-folliculitis may also present with inflamed, painful, deep-seated nodules and pustules [10].

Fungal folliculitis — After S. aureus, fungi are the most common causes of infectious folliculitis. Malassezia species, dermatophytes, and Candida albicans can cause fungal folliculitis.

Malassezia (Pityrosporum) folliculitis

●Etiology and risk factors – Multiple species of Malassezia, lipophilic yeasts present in the normal cutaneous flora, cause folliculitis. The most common species are Malassezia globosa, Malassezia sympodialis, Malassezia furfur, and Malassezia restricta [11]. These fungi were previously classified under the genus Pityrosporum (Pityrosporum orbiculare, Pityrosporum ovale, and Pityrosporum pachydermatis), contributing to the alternative name "Pityrosporum folliculitis" [12].

High sebum production and increased sweating are both predisposing factors for Malassezia folliculitis [11]. In accordance with this, Malassezia folliculitis may be more likely to occur in hot, humid climates. In a review of 44 patients with Malassezia folliculitis in Japan, 75 percent reported onset during the summer months [13].

Other potential predisposing factors include topical or oral antibiotic use, topical or oral corticosteroid treatment, and immunosuppression [13-17].

●Clinical manifestations – Malassezia folliculitis presents with pruritic, monomorphic, follicular papules or pustules on the chest, back, and/or shoulders (picture 4A-B). Other potential sites of involvement include the face, neck, and extensor side of the arms. In patients with facial involvement, lesions typically occur on the forehead, chin, and sides of the face [11,17]. The central face is usually spared.

Dermatophytic folliculitis

●Etiology and risk factors – Trichophyton, Epidermophyton, and Microsporum species are the usual causes of dermatophytic folliculitis. Tinea capitis (dermatophytic infection of the scalp) and tinea barbae (dermatophytic infection of the beard or mustache areas) are classic forms of dermatophytic infection involving hair follicles. Tinea capitis is reviewed in detail separately. (See "Tinea capitis".)

Majocchi's granuloma is a clinical subtype of dermatophytic 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 Trichophyton rubrum [3]. Predisposing factors include shaving of the legs, topical corticosteroid use, and immunocompromised status [18].

●Clinical features – Tinea barbae and Majocchi's granuloma often manifest as follicular pustules surrounded by an erythematous plaque (picture 1C, 1F-J). Hair loss in the affected site is common. Clinical features of tinea capitis are reviewed separately. (See "Tinea capitis", section on 'Clinical manifestations'.)

The most common presentation of Majocchi's granuloma is a unilateral eruption on the lower extremity (picture 1C, 1J). The upper extremities, specifically the forearm and dorsal hand, are additional common locations. Patients may have associated findings of tinea corporis, tinea cruris, or tinea pedis in other body areas.

Candidal folliculitis

●Etiology and risk factors – Cutaneous C. albicans infection may cause fungal folliculitis. Candida folliculitis has occurred in association with candidemia in intravenous drug users but also occurs in healthy individuals [3]. Immobility can produce an artificially moist, occlusive environment and lead to Candida folliculitis (eg, the occurrence of candidal folliculitis on the back of a nonambulatory, postoperative patient).

●Clinical features – Candida folliculitis has been described as a widely distributed, pustular folliculitis as well as localized, inflammatory, papulopustular eruptions in the beard, mustache, scalp, or other hair-bearing areas, including the trunk (picture 5A-B) [3,19,20]. Beard involvement can mimic tinea barbae, manifesting as a fluctuant plaque on the face with follicular pustules and papules [21].

Viral folliculitis — Viral folliculitis is most commonly associated with herpesvirus infections. Molluscum contagiosum virus (MCV) is a less common cause of viral folliculitis.

Herpetic folliculitis

●Etiology and risk factors – Herpetic folliculitis is a rare manifestation of herpesvirus infections. It is most commonly associated with varicella zoster virus (VZV) infection but also can be attributed to herpes simplex virus (HSV) 1 or HSV-2. HSV is less likely than VZV to target the hair follicle [22].

●Clinical manifestations – Erythematous papules, pustules, vesicles, papulovesicles, and plaques are the most common presentations of herpetic folliculitis (picture 6A-B) [22,23]. These lesions are often grouped or clustered [23]. HSV folliculitis in the beard area (herpetic sycosis) is reported most commonly in immunocompromised patients but may also occur in the absence of immunosuppression [24,25].

Molluscum folliculitis

●Etiology and risk factors – MCV is a poxvirus that preferentially affects children and immunocompromised adults but also occurs in healthy adults. MCV is a rare cause of viral folliculitis [26-28]. (See "Molluscum contagiosum".)

●Clinical features – Inflamed papules and pustules appearing in conjunction with the characteristic umbilicated papules of molluscum contagiosum are typical findings in molluscum folliculitis. Molluscum folliculitis is distinct from the frequent occurrence of erythema and swelling of molluscum lesions prior to clinical resolution. (See "Molluscum contagiosum", section on 'Inflamed lesions'.)

Noninflamed, pearly, and nonumbilicated papules have been reported as an alternative manifestation [29]. Presentations resembling tinea barbae and pseudolymphoma have also occurred [24-26].

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 [30,31]:

●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 the Demodex organism [32]. Support for a pathogenic role in folliculitis and rosacea stems from improvement in these disorders with anti-Demodex therapies [3].

Demodex folliculitis is most frequently diagnosed in adults. However, Demodex folliculitis has also been implicated in facial pustules and papules in children [33]. Immunosuppression, particularly related to HIV infection, may increase risk for cutaneous manifestations of Demodex infection [34].

●Clinical manifestations – Demodex folliculitis is usually characterized by rosacea-like, inflammatory papules and pustules on the face and neck (picture 7) [32]. In addition, nodulocystic and conglobate (abscess-like) presentations have occurred [35]. Demodex folliculitis is often first suspected when patients with a rosacea-like, papulopustular eruption fail to respond to antibiotic therapy for rosacea.

DIAGNOSIS — Folliculitis is usually suspected based upon the patient history and physical examination. Identification of the causative organism confirms the diagnosis:

●Bacterial folliculitis – Staphylococcal and pseudomonal folliculitis are usually diagnosed by means of the patient history and physical examination. Further work-up is primarily reserved for patients without findings that strongly suggest these diagnoses and treatment-resistant disease.

A Gram stain and culture of the contents of a pustule can confirm the presence of bacterial infection and identify the causative organism. (See "Approach to Gram stain and culture results in the microbiology laboratory".)

Infrequently, a skin biopsy is necessary to differentiate bacterial folliculitis from other skin conditions. Histopathologic examination of bacterial folliculitis shows neutrophils infiltrating a hair follicle (picture 8) [4].

●Fungal folliculitis – Fungal folliculitis may be confirmed with a potassium hydroxide (KOH) preparation, fungal culture, or skin biopsies. A periodic acid-Schiff (PAS) or Gomori methenamine silver (GMS) stain may be performed to highlight fungal elements in skin biopsy specimens:

•Malassezia folliculitis – A KOH preparation is often sufficient to confirm a diagnosis of Malassezia folliculitis. Samples for the preparation can be obtained through superficial scraping of a pustule. The detection of budding spores and short, curved hyphae, similar to those seen in tinea versicolor (picture 9), supports the diagnosis. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

A skin biopsy may also detect fungal forms consistent with Malassezia and can be useful when suspicion for Malassezia folliculitis remains despite a negative KOH preparation (picture 10). Clinical correlation is important because Malassezia can be seen in normal hair follicles.

Cultures for Malassezia are not routinely performed because Malassezia is difficult to culture without specialized media.

•Dermatophytic folliculitis – Although a KOH preparation that detects septate hyphae consistent with dermatophyte infection confirms a diagnosis of dermatophytic folliculitis, negative tests are not uncommon and do not rule out the diagnosis. The ideal sample for a KOH preparation includes hairs plucked from the involved area and scrapings of associated scale. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

If a KOH preparation cannot be performed or is negative, alternative methods for diagnosis include skin biopsy and fungal culture. Skin biopsies are often preferred for Majocchi's granuloma, as the presence of dermatophytes is easily and relatively quickly confirmed on histopathology (picture 11). However, for tinea barbae, the desire to avoid scarring on the face may favor performance of a fungal culture rather than skin biopsy. A disadvantage of fungal cultures is that results may not be available for a few weeks.

The approach to the diagnosis of tinea capitis is reviewed in detail separately. (See "Tinea capitis", section on 'Diagnosis'.)

•Candida folliculitis – Candida folliculitis may be diagnosed via a KOH preparation. The detection of yeast cells and pseudohyphae suggests Candida infection (picture 12) [21]. Fungal cultures and skin biopsies are generally reserved for confirming the diagnosis in cases in which the KOH preparation is negative or cannot be performed.

●Viral folliculitis – Additional tests are indicated to confirm a diagnosis of herpetic folliculitis. In contrast, clinical examination is typically sufficient for the diagnosis of molluscum folliculitis:

•Herpetic folliculitis – Testing of skin lesions should be performed to confirm varicella zoster virus (VZV) or herpes simplex virus (HSV) infection if a diagnosis of herpetic folliculitis is suspected [23]. Options for testing include viral culture, polymerase chain reaction (PCR), or immunofluorescence testing. (See "Diagnosis of varicella-zoster virus infection" and "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection", section on 'Tests to confirm the diagnosis'.)

A skin biopsy is not usually necessary but may also detect findings consistent with herpetic folliculitis, such as intranuclear viral inclusions with multinucleated giant cells in and around the follicular epithelium.

•Molluscum folliculitis – The presence of umbilicated papules in the region of folliculitis suggests molluscum folliculitis, and the physical examination is usually sufficient for diagnosis. A skin biopsy can be helpful when the diagnosis is unclear. Skin biopsies will reveal characteristic molluscum bodies (Henderson-Patterson bodies) in the follicular epithelium [26]. (See "Molluscum contagiosum", section on 'Diagnosis'.)

●Demodex folliculitis – A KOH preparation of a skin scraping from an involved area is typically used to detect Demodex mites (picture 13). A skin biopsy is not usually necessary but may also detect Demodex mites. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

Clinical correlation is necessary for the interpretation of the KOH preparation and skin biopsy findings 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 [32].

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 [36].

Although not routinely used for diagnosis of folliculitis, the findings of an observational study suggest dermoscopy may be a helpful, adjunctive, diagnostic tool for some forms of folliculitis [37]. (See "Overview of dermoscopy".)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of infectious folliculitis includes the various forms of infectious folliculitis (eg, bacterial, fungal, viral, Demodex) and other papular, pustular, or follicular eruptions.

Common eruptions on the face or scalp that may be confused with infectious folliculitis include:

●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 14A-B). The presence of comedones and a lack of pruritus are more consistent with acne vulgaris than folliculitis. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris".)

●Papulopustular rosacea – Papulopustular rosacea primarily affects adults and presents with pustules and erythematous papules on the central face (picture 15A-B). Exacerbating factors, such as alcohol, spicy foods, sun exposure, and temperature changes, are common. (See "Rosacea: Pathogenesis, clinical features, and diagnosis".)

●Perioral (periorificial) dermatitis – Perioral dermatitis presents with small, erythematous papules around the mouth, nose, or periorbital areas (picture 16A-B). There may be associated mild scale. Perioral dermatitis is most common in young women. (See "Perioral (periorificial) dermatitis".)

●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 17). (See "Acne keloidalis nuchae: Pathogenesis, clinical manifestations, and diagnosis".)

●Pseudofolliculitis barbae – Pseudofolliculitis barbae is an inflammatory reaction to hair penetrating interfollicular skin. Patients develop inflamed papules and pustules following hair removal in the beard area of the face or neck (picture 18). Pseudofolliculitis barbae is most common in patients of African descent. (See "Pseudofolliculitis barbae".)

Common eruptions in the differential diagnosis that most frequently affect the trunk or extremities include:

●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 19A-B) [30]. Other drugs that may cause folliculitis-like eruptions include phenytoin, lithium, isoniazid, cyclosporine, halogens, and epidermal growth factor receptor inhibitors (picture 20). (See "Acneiform eruption secondary to epidermal growth factor receptor (EGFR) and MEK inhibitors" and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acneiform eruptions'.)

●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 21A-B). Keratosis pilaris is most commonly seen in children and young adults. (See "Keratosis pilaris".)

●Hidradenitis suppurativa – Hidradenitis suppurativa is a chronic, inflammatory skin disorder characterized by the development of inflamed nodules, abscesses, and sinus tracts (picture 22). Involvement primarily occurs in the axillary, mammary, and inguinal areas. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)

●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 23). (See "Scabies: Epidemiology, clinical features, and diagnosis".)

●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 24). Histopathology demonstrates focal, acantholytic dyskeratosis that is not centered upon hair follicles. (See "Grover's disease (transient and persistent acantholytic dermatosis)".)

Other disorders in the differential diagnosis include irritant folliculitis, actinic folliculitis, eosinophilic folliculitis, and perforating folliculitis. (See "Perforating dermatoses", section on 'Perforating folliculitis'.)

MANAGEMENT — The etiology of folliculitis determines the best approach to treatment. (See 'Bacterial folliculitis' below and 'Fungal folliculitis' below and 'Viral folliculitis' below and 'Demodex folliculitis' below.)

Bacterial folliculitis — The therapeutic approach to staphylococcal folliculitis, pseudomonal folliculitis, and other forms of gram-negative folliculitis differ. (See 'Staphylococcal folliculitis' below and 'Pseudomonal folliculitis' below and 'Other gram-negative folliculitis' below.)

Staphylococcal folliculitis — Because S. aureus folliculitis is the most common form of infectious folliculitis, patients with findings suggestive of this diagnosis are often assumed to have S. aureus infection and managed accordingly. Reassessment of the diagnosis is indicated when patients fail to respond to treatment (see 'Diagnosis' above):

●General approach to treatment – Treatment of staphylococcal folliculitis is not always necessary; mild folliculitis with few pustules often resolves spontaneously. In this scenario, we often suggest daily washing of the affected area with an antimicrobial cleanser, such as benzoyl peroxide, in an attempt to accelerate improvement; however, the efficacy of this approach has not been confirmed in clinical trials.

Typical indications for antibiotic treatment include:

•Extensive disease (numerous papules or pustules or with involvement of more than one body area)

•Persistent disease (folliculitis that does not resolve spontaneously within several weeks)

Treatment with a topical antistaphylococcal antibiotic is usually sufficient for patients with limited skin involvement based upon clinical experience [38]. We typically treat with topical mupirocin three times daily for five to seven days or topical clindamycin gel, lotion, or solution twice daily for 7 to 10 days.

Other treatment options include topical retapamulin and topical fusidic acid [39]. However, increasing resistance of S. aureus to fusidic acid has been observed in areas where fusidic acid use is common, and the drug is not available in the United States [40].

Topical erythromycin has fallen out of favor due to increasing prevalence of erythromycin resistance and community-acquired methicillin-resistant Staphylococcus aureus (MRSA) infections [1].

●Extensive, recurrent, or refractory folliculitis and folliculitis (sycosis) barbae – Patients with extensive skin involvement, staphylococcal folliculitis that is recurrent or refractory after topical therapy, or folliculitis barbae are usually treated with oral antibiotics. A 7- to 10-day course is usually sufficient.

In our experience, staphylococcal folliculitis, particularly of the scalp or trunk, is sometimes persistent or recurrent despite treatment. There are insufficient data to confirm the best approach to refractory staphylococcal folliculitis. In clinical practice, these patients are often given extended courses of oral antibiotics (eg, one month or longer). Selection of the antibiotic should be based upon culture and antibiotic sensitivity results. We often use doxycycline in this scenario. Measures to prevent recurrences may also be implemented.

Due to the high frequency of resistance to penicillin, other beta-lactam antibiotics, such as dicloxacillin or cephalexin, are first-line systemic treatments when MRSA infection is not suspected [4,41]. (See "Penicillin, antistaphylococcal penicillins, and broad-spectrum penicillins".)

Typical adult dosing is as follows:

•Dicloxacillin (250 to 500 mg four times per day)

•Cephalexin (250 to 500 mg four times per day)

If MRSA is cultured or suspected (table 1), suggested treatments for adults include the following:

•Doxycycline (100 mg twice daily)

•Trimethoprim-sulfamethoxazole (one to two double-strength tablets twice daily)

•Clindamycin (450 mg three times per day)

Occasionally, treatment for more than two weeks is required for resolution of MRSA folliculitis [1]. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections".)

●Prevention – The best approach to the prevention of recurrence is unclear. Reduction of predisposing factors for folliculitis (eg, occlusive clothing, hyperhidrosis) may be beneficial. In our experience, wearing loose-fitting clothing, particularly during exercise, and changing shirts after activities with excessive sweating seem to be helpful. We often also advise daily use of an antimicrobial cleanser, such as a cleanser containing benzoyl peroxide or a stabilized hypochlorous acid wash; however, the efficacy of this approach is unclear.

Decolonization regimens have been suggested for patients with recurrent abscesses in an attempt to reduce recurrences [42]. However, data are insufficient to confirm efficacy of such measures for recurrent staphylococcal folliculitis. We generally limit decolonization to patients with recurrent MRSA skin infections. Decolonization regimens are reviewed in detail separately. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Prevention and control", section on 'Decolonization' and "Methicillin-resistant Staphylococcus aureus (MRSA) in children: Prevention and control", section on 'Decolonization regimens'.)

Pseudomonal folliculitis — Gram-negative folliculitis due to Pseudomonas is often self-limiting and resolves within 7 to 10 days with just good skin hygiene and avoidance of re-exposure to the source of infection (ie, contaminated water). Thus, treatment is not necessary for most patients.

Patients with severe presentations (extensive skin involvement or disabling pruritus) may be treated with oral ciprofloxacin (adult dose: 250 to 750 mg twice daily) [3]. Data are insufficient to determine the optimal treatment duration; we consider a seven-day treatment course reasonable.

Proper chlorination of pools and hot tubs prevents reinfection.

Other gram-negative folliculitis — Selection of an antibiotic for other forms of gram-negative folliculitis should be guided by antibacterial susceptibility testing of the causative organism. (See "Overview of antibacterial susceptibility testing".)

Common first-line treatment regimens for adults include:

●Ampicillin (250 to 500 mg four times daily)

●Trimethoprim-sulfamethoxazole (one double-strength tablet twice daily)

●Ciprofloxacin (250 to 750 mg twice daily)

Treatment for two weeks is usually sufficient, although longer courses may be appropriate for patients who have incomplete clearance at the end of this period.

Oral isotretinoin (0.5 to 1 mg/kg daily for four to five months) is the treatment of choice for recalcitrant disease [10,43]. (See "Oral isotretinoin therapy for acne vulgaris".)

Fungal folliculitis — The approach to the treatment of fungal folliculitis depends on the etiology. Oral antifungal agents such as terbinafine, 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 [44].

Malassezia folliculitis — Treatment options for Malassezia folliculitis include both oral antifungal drugs (eg, fluconazole, itraconazole) and topical antifungal drugs (eg, azole antifungal drugs, selenium sulfide). The efficacy of terbinafine for this indication is unclear:

●General approach – Oral therapy is often considered more effective than topical therapy based upon the theory that systemic therapy may eliminate Malassezia deep within hair follicles [44]. However, superiority of systemic therapy is not confirmed.

The best regimens for treatment are unclear. Examples of reasonable systemic approaches include:

•Oral fluconazole (100 to 200 mg per day for one to four weeks or 300 mg once weekly for one to two months [44])

•Oral itraconazole (200 mg per day for one to three weeks [44])

We usually treat with oral fluconazole based upon the drug's more favorable side effect profile and lower risk for drug interactions compared with itraconazole.

Examples of reasonable topical regimens include:

•Ketoconazole shampoo applied for five minutes three to four times per week for approximately one month

•Topical azole antifungal agent (eg, ketoconazole, clotrimazole, econazole) applied once or twice daily for approximately one month (table 2)

Large, high-quality studies evaluating the efficacy of treatments are lacking. One small, randomized trial (n = 26) found oral itraconazole (200 mg per day for one week) superior to placebo (clinical clearance in 69 versus 0 percent and negative potassium hydroxide [KOH] preparation in 85 versus 8 percent after five weeks) [45].

Uncontrolled and retrospective studies also support benefit of oral fluconazole and topical antifungal treatments, such as topical ketoconazole shampoo, ketoconazole cream, econazole cream, selenium sulfide shampoo, and propylene glycol 50% in water, for achieving improvement or resolution. [13,17,46]. In contrast, poor efficacy of topical azole antifungal drug monotherapy was reported in a study that compared outcomes from treatment with oral ketoconazole (alone or in conjunction with ketoconazole shampoo), econazole nitrate 1% solution, and miconazole nitrate 1% cream in 62 patients with Malassezia folliculitis [47].

●Prevention of recurrence – 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 performed in an attempt to prevent recurrence of disease [37,47].

●Other interventions – Although not typically indicated, improvement of Malassezia folliculitis with isotretinoin or photodynamic therapy has been reported [44,48,49].

Dermatophytic folliculitis — Dermatophytic folliculitis must be treated with systemic therapy. Topical antifungals may help to reduce transmission of infection but are usually ineffective for treatment due to insufficient penetration of the hair follicle:

●Tinea barbae and Majocchi's granuloma – Oral terbinafine is our preferred first-line treatment of tinea barbae and Majocchi's granuloma. We typically treat adults with oral terbinafine (250 mg per day) for four weeks, with the precise duration of treatment determined based upon clinical response. Treatment is continued until complete clinical resolution. Case reports and case series describe resolution of disease with doses ranging from 250 to 500 mg of terbinafine per day for four to six weeks or longer [18,50-53].

Oral griseofulvin and itraconazole are also considered effective for dermatophytic folliculitis and are alternatives to terbinafine [3,18,54,55]. A case series of seven successfully treated patients with Majocchi's granuloma suggests efficacy of pulse therapy with itraconazole (up to three pulses of 200 mg twice daily for one week followed by two weeks off therapy) [54].

Our typical regimen for griseofulvin therapy for adults treated is 500 mg daily (microsize) for four to eight weeks. Our preferred regimen for itraconazole is 200 mg twice daily for one week per month for one to three months.

●Tinea capitis – The management of tinea capitis is reviewed separately. (See "Tinea capitis", section on 'Treatment'.)

Candida folliculitis — Candida folliculitis can be treated with oral fluconazole or itraconazole. Oral terbinafine is not effective [3,21]. Our typical approach for localized Candida folliculitis is to give fluconazole 150 mg per week for two to four weeks or fluconazole 50 mg per day for four weeks.

However, data on the treatment of localized Candida folliculitis are limited and insufficient to determine the most appropriate approach to treatment. Examples of regimens that have been associated with improvement in case reports or small case series include fluconazole 100 mg per day for one week followed by every other day for one month, fluconazole 50 mg per day for four weeks, and itraconazole 200 mg per day for two weeks [20,21,56].

Patients with associated candidemia should be treated accordingly. (See "Management of candidemia and invasive candidiasis in adults" and "Candidemia and invasive candidiasis in children: Management".)

Viral folliculitis — The therapeutic approaches for herpetic folliculitis and molluscum folliculitis differ.

Herpetic folliculitis — Herpetic folliculitis should be treated with systemic antiviral therapy.

Data on treatments for herpes folliculitis are limited, and the most appropriate regimens for antiviral therapy for herpetic folliculitis are unclear. Various dose regimens have been utilized [25,26,57,58]. We consider doses resembling those used for herpes zoster reasonable, particularly in the setting of herpes folliculitis secondary to varicella zoster virus (VZV) infection:

●Acyclovir – 800 mg five times per day for seven days

●Valacyclovir – 1 g three times daily for seven days

●Famciclovir – 500 mg three times per day for seven days

Case reports suggest lower doses or shorter courses may be effective in patients with herpes simplex virus (HSV)-related herpetic folliculitis [25,26,58]. (See "Treatment and prevention of herpes simplex virus type 1 in immunocompetent adolescents and adults".)

Molluscum folliculitis — Molluscum folliculitis can be treated similarly to classic molluscum contagiosum infection. Common treatment options for molluscum contagiosum include curettage, cantharidin, and cryotherapy. Podophyllotoxin and trichloroacetic acid are additional treatments [3]. We typically treat with cantharidin or cryotherapy. (See "Molluscum contagiosum", section on 'Overview of management'.)

Demodex folliculitis — Data on treatment options for Demodex folliculitis are limited. We typically treat with permethrin 5% cream or oral ivermectin. Additional treatment options include topical sulfur and oral metronidazole [59].

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.

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 [31]; however, further study is necessary to confirm whether combination therapy is indicated for Demodex folliculitis. The efficacy of topical ivermectin remains to be determined.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Skin and soft tissue infections".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Bacterial folliculitis (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Etiology – Folliculitis is inflammation of the superficial or deep portion of the hair follicle. Folliculitis may be infectious or noninfectious. Infectious folliculitis can be caused by bacteria, fungi, viruses, or parasites. The most common pathogen in infectious folliculitis is Staphylococcus aureus. Other common pathogens are Pseudomonas aeruginosa, Malassezia species, and Demodex mites. (See 'Introduction' above.)

●Clinical features – Follicular pustules and follicular, erythematous papules are the most common clinical findings of folliculitis. (See 'Bacterial folliculitis' above and 'Fungal folliculitis' above and 'Viral folliculitis' above and 'Demodex folliculitis' above.)

●Diagnosis – A diagnosis of folliculitis can often be made based upon the patient history and clinical findings. Further testing is necessary when the etiology is unclear. A Gram stain, bacterial culture, potassium hydroxide (KOH) preparation, viral culture, polymerase chain reaction (PCR) assay, or immunofluorescence testing can aid in diagnosis, depending on the type of folliculitis suspected. Skin biopsies are not usually necessary but may be helpful in difficult cases. (See 'Bacterial folliculitis' above and 'Fungal folliculitis' above and 'Viral folliculitis' above and 'Demodex folliculitis' above.)

●Management – The management of folliculitis varies based upon the etiology:

•Mild staphylococcal folliculitis – Mild S. aureus folliculitis may resolve without antibiotic treatment. For patients with known or suspected S. aureus folliculitis that persists and involves a limited area of skin, we suggest topical antibiotic therapy rather than oral antibiotic therapy as initial treatment (Grade 2C).

Topical mupirocin and topical clindamycin are our preferred initial treatments. (See 'Staphylococcal folliculitis' above.)

•Extensive staphylococcal folliculitis – For patients with extensive S. aureus folliculitis, S. aureus folliculitis that fails to resolve or recurs after topical treatment, or folliculitis barbae, we suggest systemic antibiotic therapy rather than topical antibiotic therapy (Grade 2C).

Appropriate initial treatment options include dicloxacillin and cephalexin. If methicillin-resistant Staphylococcus aureus (MRSA) is suspected, patients should be treated with trimethoprim-sulfamethoxazole, clindamycin, or doxycycline. (See 'Staphylococcal folliculitis' above.)

•Other types of folliculitis – Oral antifungal therapy is the mainstay of therapy for fungal folliculitis. Antiparasitic agents, such as permethrin and oral ivermectin, can be effective for Demodex folliculitis. (See 'Fungal folliculitis' above and 'Demodex folliculitis' above.)