Folliculitis

Back

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 Conglobata, Acne Fulminans, Acne Keloidalis Nuchae, Acne 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:

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.  

History

Patients with superficial folliculitis typically report an acute onset associated with pruritus or mild discomfort. 

Patients with deep folliculitis usually have longer-standing lesions and more often report pain and sometimes suppurative drainage. Persistent or recurrent lesions may result in scarring and permanent hair loss. Patients may also develop folliculitis following laser epilation.[21]

The follicular papulopustular eruption secondary to epidermal growth factor receptor inhibitors usually presents within the first 2-weeks of initiation of therapy. Typically it occurs on the face, scalp, chest, and upper back and is often associated with pruritus, pain, and desquamation. The eruption is dose-dependent and peaks after 3-4 weeks of therapy. Although, the eruption can negatively affect the quality of life of some patients, some authors believe the acneiform eruption also seems to correlate with a good response to therapy.[15, 16]

Physical Examination

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, tender 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. Anatomic location can help narrow down etiology. Scalp folliculitis most often is due to to traction or other minor trauma, occulsion, Staphylococcus aureus, Malassezia, or dermatophyte; Facial follicultis is most often due to occulsion, medication-induced,  minor trauma/ingrown hair, Staphylococcus aureus, Malassezia, Demodex, Candida, Herpes, dermatophyte or gram negative folliculits (due to prolonged antibotics); whereas Truncal folliculitis most commonly due to occulsion, medication-induced, Staphylococcus aureus, Pseudomonas (hot tub folliculitis), Malassezia, dermatophyte (tinea incognito/Majocchi granuloma), molluscum, or Candida.

The most common superficial form of infectious folliculitis is known as impetigo of Bockhart, barbers itch, or folliculitis barbae and is caused by Staphylococcus aureus, such as the infection shown in the image below.[10, 30] The lesions are seen in the bearded area, often on the upper lip near the nose, as erythematous follicular-based papules or pustules that occur in crops and may rupture leaving 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.[30]



View Image

A 22-month-old boy with a staphylococcal folliculitis on the buttocks. The lesions have been excoriated. Diaper occlusion may have been related to ons....

When involvement of the follicle is more extensive, a follicular-centered dermal abscess develops. When this occurs in the beard areas of 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.[1, 30]

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 who have direct contact with an animal 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 type of deep fungal folliculitis called Majocchi granuloma classically occurs after treatment of a superficial fungal infection with steroids and occlusion or on the legs of women from shaving.

Gram-negative folliculitis primarily occurs in patients on long-term antibiotic therapy, most often in patients treated for 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,Morganella,[33] 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. Approximately 4% of acne patients treated with systemic antibiotics develop gram-negative folliculitis.[30, 34]

Pseudomonal folliculitis is another gram-negative folliculitis and is also known as hot tub (spa) folliculitis and wet suit folliculitis (see the images below). It appears 8-48 hours after exposure to contaminated water or wet suits as erythematous follicular-based papules and pustules that are most concentrated in areas occluded by swimwear. This form of folliculitis may be associated with systemic findings such as fever, headache, sore throat, malaise, or gastrointestinal distress, but it is a self-limited condition that resolves in 7-14 days. Aeromonas folliculitis is also associated with water exposure.[35]

Another similar condition is Pseudomonas hot hand-foot syndrome, which occurs in a similar clinical situation but eventuates in painful erythematous nodules and papules on the palms and soles rather than folliculitis.[27]



View Image

A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.



View Image

Pseudomonas folliculitis. Courtesy of Hon Pak, MD.

Pityrosporum folliculitis, typically seen in young adults, with a slight female predominance, presents as intensively pruritic small uniform papules and pustules on the back, chest, and shoulders. Facial involvement may resemble monomorphous acne and may have less pruritus.[32] 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.[31]

Candida folliculitis due to C. albicans affects the scalp, face, trunk and pubis and manifests as a pustular or papular rash.  It is rare and should be considered in patients with a history of recurrent candidiasis.[36]

An unusual cause of folliculitis occurs as a result of Demodex mites, either due to increased density of these commensal saprophytic mites or due to an acquired hypersensitivity reaction. This form of folliculitis manifests with a more diffuse background erythema, in addition to the follicular-centered papules and pustules which are most concentrated in seborrehic regions of face, and less commonly can occur on chest, back and genital region.[37, 38, 39]

An uncommon form of folliculitis is due to an infection with herpes viruses or molluscum. 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.[40, 41]

Varicella-zoster virus may present with exclusive follicular involvement.  Most patients present with erythematous hyperkeratotic papules in a dermatomal distribution; however, dissemination can occur in immunocompromised patients.[42] In contrast to the characteristic lesions seen in most herpes infections, vesicles typically do not occur. Biopsy is often required to confirm the diagnosis.[41]

Folliculitis can also have a noninfectious etiology caused by follicular trauma or occlusion or may 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.[12] 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.[10]

A uncommon, non-infectious cause of folliculitis is actinic folliculitis with presents most frequently in females as an acute eruption of non-pruritic monomorphic pustules overlying an erythematous base on face and trunk within 4-48hrs after sun-exposure. [10, 17, 18]

Acne keloidalis nuchae is a similar condition that arises on the neck and occipital region of the scalp. This condition tends to be more chronic and has greater potential for scarring.[10]   

Perifolliculitis capitis abscedens et suffodiens, also known as dissecting cellulitis of the scalp (DCS) and Hoffman disease, is a chronic form of deep folliculitis which most often occurs in African American males which is characterized by perifollicular pustules, fluctuating, interconnecting nodules and ultimately eventuates in cicatricial alopecia.[43]

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.[13, 14, 44] Effective management can be critical to compliance with the anticancer treatment regimen.

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 pustular folliculitis, also known 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; however, granulomatous lesions have also been described.[6] 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.[29]

A second form of eosinophilic folliculitis arises in patients with AIDS and other conditions that result in immunosuppression.[45] 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.[4] Eosinophilic folliculitis may also occur after antiretroviral therapy, possibly through macrophage activation.[5]

The last form of eosinophilic folliculitis occurs in infants. 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. Unlike the adult form, the lesions primarily affect the scalp and eyebrows and are often associated with secondary crusting. This form may also be associated with peripheral eosinophilia.

 

Complications

Complications from folliculitis are uncommon; however, persistent and deep folliculitis can result in cellulitis, furunculosis, scarring, sinus tract formation, and permanent hair loss.

Laboratory Studies

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 gram stain, cultures, potassium chloride (KOH) preparation or 3-4mm punch biopsy may be required to determine exact etiology in atypical cases or in patients resistant to standard treatments. 

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 Malassezia (Pityrosporum) folliculitis.

Viral culture or punch biopsy can assist in the identification of folliculitis caused by herpes simplex virus.

A complete blood cell count often reveals leukocytosis and eosinophilia, with elevated immunoglobulin E levels in patients with eosinophilic folliculitis.

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.[46] Note the image below.



View Image

Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle

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, as demonstrated in the image below.



View Image

Perifolliculitis, showing inflammatory cells 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.[40]

In pseudofolliculitis barbae and acne keloidalis nuchae, the inflammatory infiltrate is initially perifollicular and is composed of neutrophils and lymphocytes; however, later, the predominant cells are 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.[46]

The light microscopic features of eosinophilic folliculitis include perifollicular infiltrates of lymphocytes and eosinophils associated with follicular eosinophilic spongiosis. This type of folliculitis is often associated with follicular mucinosis.[29]

The histological features of a papulopustular eruption due to epidermal growth factor receptor inhibitors is that of a superficial purulent folliculitis, which, in most cases, is sterile but can occasionally be associated with S aureus infection.[14]

Medical Care

It is essential to determine presumptive etiology based on clinical history, morphology and distribution of the lesions, along with severity before a treatment plan is devised. For uncomplicated superficial folliculitis, use of antimicrobial cleansers such as benzoyl peroxide and good hand-washing techniques may be all that is needed. Lesions which are more inflamed often respond well to warm compresses with or without the use of a topical antistaphylococcal agent. For refractory or deep lesions where an infectious etiology is suspected, empiric treatment with oral antibiotics that cover gram-positive organisms should be considered. For patients who do 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 since it is the most common pathogen. Because this organism may be penicillin resistant, dicloxacillin or a cephalosporin are the initial choices of therapy. Methicillin-resistant organisms are becoming more common, and treatment may require clindamycin, trimethoprim-sulfamethoxazole, minocycline, or linezolid.

Deep folliculitis is best approached with warm compresses, followed by incision and drainage once a conical pustular head develops. For recurrent and recalcitrant folliculitis, in addition to oral antibiotics, a search for a bacterial reservoir is important. Mupirocin ointment in the nasal vestibule twice a day for 5 days may eliminate the S aureus carrier state. Family members may also 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:

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.

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.  Do not share razors with other members of the household.

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. 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.

In cases of acute infectious 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.

Medication Summary

Topical antibiotics can be used as first-line agents in cases of recurrent superficial folliculitis. If a patient has widespread involvement, persistent lesions, or if a deep infection is present, systemic antibiotics may then be indicated. The drug of choice must cover penicillin-resistant S aureus or, in some situations, methicillin-resistant S aureus.

Clindamycin, topical (Cleocin, Cleocin T, ClindaMax, Clindagel, Evocin)

Clinical Context:  Clindamycin topical solution is a lincosamide for the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Mupirocin (Bactroban, Centany)

Clinical Context:  Mupirocin is the drug of choice for localized disease; it inhibits bacterial growth by inhibiting RNA and protein synthesis.

Cephalexin (Keflex)

Clinical Context:  Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. It has primary activity against skin flora and is used for skin infections or prophylaxis in minor procedures.

Although cephalosporins have significant staphylococcal coverage in most populations, coverage of Pasteurella species is not as good as amoxicillin and clavulanate.

Dicloxacillin

Clinical Context:  Dicloxacillin is for the treatment of infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when staphylococcal infection is suspected.

Erythromycin topical (Akne-mycin, Ery)

Clinical Context:  Erythromycin inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of staphylococcal and streptococcal infections. This topical solution (2%) is indicated for infections caused by susceptible strains of microorganisms.

Minocycline (Minocin, Dynacin, Solodyn)

Clinical Context:  Minocycline is not the drug of choice for staphylococcal infection. It treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma species. Minocycline was found to be effective in some nontuberculotic mycobacterial infections.

Rifampin (Rifadin)

Clinical Context:  Rifampin is for use in combination with at least one other anti-TB drug. It inhibits DNA-dependent bacterial RNA polymerase but not mammalian RNA polymerase. Cross-resistance may occur. Treat for 6-9 months or until 6 months have elapsed from conversion to sputum culture negativity.

Ciprofloxacin (Cipro)

Clinical Context:  Ciprofloxacin inhibits DNA gyrase and topoisomerase IV for bactericidal activity. Use it as an alternative for MRSA infection.

Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

Clinical Context:  Trimethoprim/sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. The antibacterial activity of trimethoprim/sulfamethoxazole includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Linezolid (Zyvox)

Clinical Context:  Linezolid binds to the 50S ribosomal subunit, interfering with protein synthesis. This agent is used for MRSA or complicated skin infections.

Dapsone (Aczone)

Clinical Context:  Dapsone prevents bacterial use of para-aminobenzoic acid (PABA) for folic acid synthesis by acting as a competitive inhibitor. It is used in the treatment of eosinophilic pustular folliculitis.

Class Summary

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

Indomethacin (Indocin)

Clinical Context:  Indomethacin is a potent inhibitor of cyclooxygenase, which may decrease the local production of arachidonic acid–derived chemotactic factors for eosinophils present in sebum (eg, 12-L-hydroxy-5,8,10-heptadecatrienoic acid and/or prostaglandin).

Class Summary

Because the etiology and the pathogenesis of eosinophilic pustular folliculitis have not been fully elucidated, no established treatment schemes exist. A number of options have been tried with various results; however, no controlled treatment trials have been performed for this condition. Oral indomethacin consistently appears to be most beneficial, at least in the classic form of the disease.

Ciclopirox (Loprox)

Clinical Context:  Ciclopirox interferes with DNA, RNA, and protein synthesis by inhibiting the transport of essential elements in fungal cells.

Econazole topical (Ecoza)

Clinical Context:  Econazole is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. It disrupts fungal cell wall permeability, causing fungal cell death.

Ketoconazole (Nizoral, Xolegel, Extina)

Clinical Context:  Ketoconazole is an imidazole broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal death.

Class Summary

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.

Antifungals are used in the first-line therapy of Pityrosporum folliculitis. The use of topical agents has few adverse effects besides an allergic reaction to the active agent or inactive component. The mechanism of action usually involves the inhibition of pathways (eg, enzyme, substrate, transport) that are necessary for sterol and/or cell membrane synthesis, or the permeability of the cell membrane (polyenes) of the fungal cell is altered.

Famciclovir (Famvir)

Clinical Context:  Famciclovir is a prodrug that, when biotransformed into the active metabolite penciclovir, may inhibit viral DNA synthesis/replication.

Valacyclovir (Valtrex)

Clinical Context:  Valacyclovir is a prodrug that is rapidly converted to the active drug acyclovir. It is more expensive than acyclovir, but its dosing regimen is more convenient.

Acyclovir (AHydrocort, Alphosyl, Aquacort)

Clinical Context:  Acyclovir has an affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain termination when acted upon by DNA polymerase. The drug, which requires 5 daily doses, can be associated with compliance problems.

Class Summary

These agents are inhibitors of DNA polymerase in HSV-1 and HSV-2 strains, inhibiting viral replication. They are used in folliculitis secondary to herpes viral infections.

What is folliculitis?How are superficial and deep folliculitis characterized?How is perifolliculitis defined?What is the role of acne in folliculitis?What causes folliculitis?What causes eosinophilic folliculitis?What is the pathophysiology of papulopustular eruption in folliculitis?What causes folliculitis?What is the incidence of folliculitis?What are the racial predilections of folliculitis?How does the incidence of folliculitis vary by sex?How does the incidence of folliculitis vary by age?What are the signs and symptoms of superficial folliculitis?What are the signs and symptoms of deep folliculitis?What are the signs and symptoms of follicular papulopustular eruption caused by EGFR inhibitor therapy?What are the physical findings characteristic of folliculitis?What causes follicular-centered dermal abscess in folliculitis?What is the role of tinea barbae in the etiology of folliculitis?What are the physical findings characteristic more severe folliculitis?What are the physical findings characteristic of gram-negative folliculitis?What are the physical findings characteristic of pseudomonal folliculitis?What are the physical findings characteristic of Pityrosporum folliculitis?What are physical findings characteristic of folliculitis in immunosuppressed patients?What are the characteristics of folliculitis due to an infection with herpes viruses?What are the physical findings of folliculitis characteristic of varicella-zoster virus infection?What are the physical findings characteristic of folliculitis with a noninfectious etiology?How is acne keloidalis nuchae differentiated from folliculitis?How are acute generalized exanthematous pustulosis and anticonvulsant hypersensitivity syndrome differentiated?What are the physical findings of papulopustular drug eruption due to EGF-R?What is the manifestation of eosinophilic folliculitis?What has been found to mimic the presentation of folliculitis?What are complications from folliculitis?What are the differential diagnoses for Folliculitis?What is the role of lab studies in the workup of folliculitis?What is the role of incision and drainage in the diagnosis and management of folliculitis?Which histologic findings are characteristic of folliculitis?Which histologic findings are characteristic of herpes folliculitis?Which histologic findings are characteristic of pseudofolliculitis?Which histologic findings are characteristic of eosinophilic folliculitis?Which histologic features are characteristic of follicular papulopustular eruption caused by EGFR inhibitor therapy?What should be considered in the treatment of folliculitis?What is the role of systemic antibiotics in the treatment of folliculitis?What are the treatment options for deep folliculitis?What is the medical care for specific types of folliculitis?Which specialists should be consulted in the treatment of folliculitis?What dietary restrictions are recommended for folliculitis?What activity restrictions are recommended for folliculitis?How is folliculitis prevented?What is included in long-term monitoring of folliculitis?What can be used as first-line agents for the treatment of folliculitis?Which medications in the drug class Antivirals, Other are used in the treatment of Folliculitis?Which medications in the drug class Antifungals, Other are used in the treatment of Folliculitis?Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are used in the treatment of Folliculitis?Which medications in the drug class Antibiotics, Other are used in the treatment of Folliculitis?

Author

Elizabeth K Satter, MD, MPH, Dermatologist and Dermatopathologist

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Andrea Leigh Zaenglein, MD, Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine

Disclosure: Received consulting fee from Galderma for consulting; Received consulting fee from Valeant for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Anacor for consulting; Received grant/research funds from Stiefel for investigator; Received grant/research funds from Astellas for investigator; Received grant/research funds from Ranbaxy for other; Received consulting fee from Ranbaxy for consulting.

References

  1. Eley CD, Gan VN. Picture of the month. Folliculitis, furunculosis, and carbuncles. Arch Pediatr Adolesc Med. 1997 Jun. 151(6):625-6. [View Abstract]
  2. Stollery N. Skin infections. Practitioner. 2014 Apr. 258(1770):32-3. [View Abstract]
  3. Winters RD, Mitchell M. Folliculitis. StatPearls [Internet]. 2020 Jan. [View Abstract]
  4. Majors MJ, Berger TG, Blauvelt A, Smith KJ, Turner ML, Cruz PD Jr. HIV-related eosinophilic folliculitis: a panel discussion. Semin Cutan Med Surg. 1997 Sep. 16(3):219-23. [View Abstract]
  5. Okada S, Fujimura T, Furudate S, Kambayashi Y, Kikuchi K, Aiba S. Immunosuppression-associated eosinophilic pustular folliculitis (IS-EPF) developing after Highly Active Anti-Retroviral Therapy (HAART): the possible mechanisms through CD163+ M2 macrophages. Eur J Dermatol. 2013 Sep-Oct. 23(5):713-4. [View Abstract]
  6. Kinoshita Y, Kono T, Ansai SI, Saeki H. An aggressive case of granulomatous eosinophilic pustular folliculitis on the face. JAAD Case Rep. 2019 Mar. 5 (3):237-239. [View Abstract]
  7. Mohseni Afshar Z, Goodarzi A, Emadi SN, Miladi R, Shakoei S, Janbakhsh A, et al. A Comprehensive Review on HIV-Associated Dermatologic Manifestations: From Epidemiology to Clinical Management. Int J Microbiol. 2023. 2023:6203193. [View Abstract]
  8. Bobotsis R, Brathwaite S, Eshtiaghi P, Rodriguez-Bolanos F, Doiron P. HIV: Inflammatory dermatoses. Clin Dermatol. 2024 Mar-Apr. 42 (2):169-179. [View Abstract]
  9. Kircik LH. Advances in the Understanding of the Pathogenesis of Inflammatory Acne. J Drugs Dermatol. 2016 Jan 1. 15 (1):s7-s10. [View Abstract]
  10. Sun KL, Chang JM. Special types of folliculitis which should be differentiated from acne. Dermatoendocrinol. 2017. 9 (1):e1356519. [View Abstract]
  11. Vasam M, Korutla S, Bohara RA. Acne vulgaris: A review of the pathophysiology, treatment, and recent nanotechnology based advances. Biochem Biophys Rep. 2023 Dec. 36:101578. [View Abstract]
  12. Ogunbiyi A. Pseudofolliculitis barbae; current treatment options. Clin Cosmet Investig Dermatol. 2019. 12:241-247. [View Abstract]
  13. 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. [View Abstract]
  14. Roe E, Garcia Muret MP, Marcuello E, Capdevila J, Pallares 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. 2006 Sep. 55(3):429-37. [View Abstract]
  15. Madke B, Gole P, Kumar P, Khopkar U. Dermatological Side Effects of Epidermal Growth Factor Receptor Inhibitors: 'PRIDE' Complex. Indian J Dermatol. 2014 May. 59 (3):271-4. [View Abstract]
  16. Fabbrocini G, Panariello L, Caro G, Cacciapuoti. Acneiform Rash Induced by EGFR Inhibitors: Review of the Literature and New Insights. Skin Appendage Disord. 2015. 1:31-37.
  17. Porter AP, James WD. Acute and recurrent pustulosis: consolidating uncommon cases of follicular pustulosis induced by UV light and other triggers. Int J Womens Dermatol. 2023 Oct. 9 (3):e100. [View Abstract]
  18. Rahman S, Powell J, Al-Ismail D. First reported cases of actinic folliculitis treated successfully with topical retinoid. Clin Exp Dermatol. 2020 Aug. 45 (6):716-718. [View Abstract]
  19. Vary JC Jr, Colven R, Kirby P. Hypertrophic scars from surgical staples mimicking folliculitis. J Am Acad Dermatol. 2010 Jan. 62(1):157-8. [View Abstract]
  20. Fox GN, Stausmire JM, Mehregan DR. Traction folliculitis: an underreported entity. Cutis. 2007 Jan. 79(1):26-30. [View Abstract]
  21. Schuler A, Veenstra J, Tisack A. Folliculitis Induced by Laser Hair Removal: Proposed Mechanism and Treatment. J Clin Aesthet Dermatol. 2020 May. 13 (5):34-36. [View Abstract]
  22. Yuan C, Wang B. Acneiform eruption induced by molecularly targeted agents in antineoplastic therapy: A review. J Cosmet Dermatol. 2023 Aug. 22 (8):2150-2157. [View Abstract]
  23. Bahbouhi I, Aboudourib M, Hocar O, Amal S. Vitamin B12 induced acneiform eruption. Heliyon. 2023 May. 9 (5):e16120. [View Abstract]
  24. Sherertz EF. Acneiform eruption due to "megadose" vitamins B6 and B12. Cutis. 1991 Aug. 48 (2):119-20. [View Abstract]
  25. Bowden A, Ekeh O, Brownstone ND, Hsu S. Acneiform Eruption Secondary to Over-the-Counter Vitamin B12. Cureus. 2023 Aug. 15 (8):e43275. [View Abstract]
  26. Walsh SR, Johnson RP. Vaccinia Folliculitis After Primary Dryvax Vaccination. Infect Dis Clin Pract. 2007 Mar. 15(2):132-4.
  27. 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. 2007 Oct. 57(4):596-600. [View Abstract]
  28. Thuraisingam T, Mirmirani P. Erosive Pustular Dermatosis: A Manifestation of Immunosenescence A Report of 8 Cases. Skin Appendage Disord. 2018 Aug. 4 (3):180-186. [View Abstract]
  29. Nervi SJ, Schwartz RA, Dmochowski M. Eosinophilic pustular folliculitis: a 40 year retrospect. J Am Acad Dermatol. 2006 Aug. 55(2):285-9. [View Abstract]
  30. Laureano AC, Schwartz RA, Cohen PJ. Facial bacterial infections: folliculitis. Clin Dermatol. 2014 Nov-Dec. 32 (6):711-4. [View Abstract]
  31. Rubenstein RM, Malerich SA. Malassezia (pityrosporum) folliculitis. J Clin Aesthet Dermatol. 2014 Mar. 7 (3):37-41. [View Abstract]
  32. Tsai YC, Wang JY, Wu YH, Wang YJ. Atypical clinical presentations of Malassezia folliculitis: a retrospective analysis of 94 biopsy-proven cases. Int J Dermatol. 2018 Mar. 57 (3):e19-e20. [View Abstract]
  33. Livani F, Kabir S. Gram-negative folliculitis caused by Morganella morganii. JAAD Case Rep. 2019 Jun. 5 (6):558-559. [View Abstract]
  34. Lousada MB, Lachnit T, Edelkamp J, Rouillé T, Ajdic D, Uchida Y, et al. Exploring the human hair follicle microbiome. Br J Dermatol. 2020 Aug 6. [View Abstract]
  35. Olszewski AE, Karandikar MV, Surana NK. Aeromonas as a Cause of Purulent Folliculitis: A Case Report and Review of the Literature. J Pediatric Infect Dis Soc. 2016 Dec 16. [View Abstract]
  36. Okwuwa I, Alam N, Wai R, Shayeb M, Sanchez A, Gandhi K, et al. Pubic Candida Folliculitis, A Case Report in a Patient With Recurrent Vaginal Candidiasis. J Family Reprod Health. 2023 Mar. 17 (1):62-64. [View Abstract]
  37. Dong H, Duncan LD. Cytologic findings in Demodex folliculitis: a case report and review of the literature. Diagn Cytopathol. 2006 Mar. 34(3):232-4. [View Abstract]
  38. Alniemi DT, Chen DL. Perioral Demodex folliculitis masquerading as perioral dermatitis in the peripartum period. JAAD Case Rep. 2019 Jul. 5 (7):639-641. [View Abstract]
  39. Paichitrojjana A. Demodex: The worst enemies are the ones that used to be friends. Dermatol Reports. 2022 Sep 14. 14 (3):9339. [View Abstract]
  40. Boer A, Herder N, Winter K, Falk T. Herpes folliculitis: clinical, histopathological, and molecular pathologic observations. Br J Dermatol. 2006 Apr. 154(4):743-6. [View Abstract]
  41. Weinberg JM, Mysliwiec A, Turiansky GW, Redfield R, James WD. Viral folliculitis. Atypical presentations of herpes simplex, herpes zoster, and molluscum contagiosum. Arch Dermatol. 1997 Aug. 133(8):983-6. [View Abstract]
  42. Tilley DH, Satter EK, Kakimoto CV, Lederman ER. Disseminated verrucous varicella zoster with exclusive follicular involvement. Arch Dermatol. 2012 Mar. 148 (3):405-7. [View Abstract]
  43. Scheinfeld N. Dissecting cellulitis (Perifolliculitis Capitis Abscedens et Suffodiens): a comprehensive review focusing on new treatments and findings of the last decade with commentary comparing the therapies and causes of dissecting cellulitis to hidradenitis suppurativa. Dermatol Online J. 2014 May 16. 20 (5):22692. [View Abstract]
  44. Bensadoun RJ, Humbert P, Krutman J, Luger T, Triller R, Rougier A, et al. Daily baseline skin care in the prevention, treatment, and supportive care of skin toxicity in oncology patients: recommendations from a multinational expert panel. Cancer Manag Res. 2013. 5:401-8. [View Abstract]
  45. 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. 2006 Apr. 54(4):581-8. [View Abstract]
  46. Weedon D, Strutton G. Skin Pathology. 2nd ed. New York, NY: Churchill Livingstone; 2002. 459-66.
  47. Satoh T, Shimura C, Miyagishi C, Yokozeki H. Indomethacin-induced reduction in CRTH2 in eosinophilic pustular folliculitis (Ofuji's disease): a proposed mechanism of action. Acta Derm Venereol. 2010. 90(1):18-22. [View Abstract]
  48. Cai L, Yan Y, Li Y, Lin J, She X, Wang X. Two cases of eosinophilic pustular folliculitis successfully treated with abrocitinib. J Dermatol. 2024 May 28. [View Abstract]
  49. Li J, Wei E, Reisinger A, French LE, Clanner-Engelshofen BM, Reinholz M. Comparison of Different Anti-Demodex Strategies: A Systematic Review and Meta-Analysis. Dermatology. 2023. 239 (1):12-31. [View Abstract]
  50. Gorji M, Joseph J, Pavlakis N, Smith SD. Prevention and management of acneiform rash associated with EGFR inhibitor therapy: A systematic review and meta-analysis. Asia Pac J Clin Oncol. 2022 Dec. 18 (6):526-539. [View Abstract]
  51. Bierbrier R, Lam M, Pehr K. A systematic review of oral retinoids for treatment of acneiform eruptions induced by epidermal growth factor receptor inhibitors. Dermatol Ther. 2022 May. 35 (5):e15412. [View Abstract]

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.

A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.

Pseudomonas folliculitis. Courtesy of Hon Pak, MD.

Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle

Perifolliculitis, showing inflammatory cells surrounding the follicle,

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.

A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.

Pseudomonas folliculitis. Courtesy of Hon Pak, MD.

Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle

Perifolliculitis, showing inflammatory cells surrounding the follicle,