Folliculitis

Background

Folliculitis is defined histologically as the presence of inflammatory cells within the wall and ostia of the hair follicle, creating a follicular-based pustule. The type of inflammatory cells varies depending on the etiology of the folliculitis and/or the stage at which the biopsy specimen was obtained.^[1]

In superficial folliculitis, the inflammation is restricted to the infundibular aspect of the follicle, whereas in deep folliculitis the inflammation not only involves the deeper aspect of the follicle, it also extends into the surrounding dermis. Deep folliculitis can eventuate from chronic lesions of superficial folliculitis or from lesions that are manipulated, and may ultimately result in scarring.

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.

Acne represents a noninfectious form of folliculitis. Recently there has been a paradigm shift, and the pathogenesis of acne is now thought to be a primary inflammatory disorder since histology findings have indicated the presence of perifollicular inflammatory cells even in early stages of acne, preceding the development 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.^[2]

Acne-related Medscape articles include Acne Conglobata, Acne Fulminans, Acne Keloidalis Nuchae, Acne Vulgaris, and Acneiform Eruptions.

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Pathophysiology

Folliculitis refers to inflammation of the hair follicle. It can be caused by an infection (bacterial, viral, fungal, or parasitic) or have a noninfectious etiology, most commonly as the result of follicular trauma, inflammation, or occlusion.

Eosinophilic folliculitis has a different etiology and is thought to occur as a result of an autoimmune process directed against the sebocytes or some component of the sebum.^{[3, 4, 5]}

Although the pathophysiology of the acneiform eruption secondary to epidermal growth factor receptor inhibitors is poorly understood, it is hypothesized that the papulopustular eruption occurs secondary to inhibition of follicular epidermal differentiation, which eventuates in follicular obstruction and subsequent inflammation.^{[6, 7, 8, 9]}

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Etiology

The most common causes of folliculitis include infection (bacterial, fungal, viral, and parasitic), friction and other causes of follicular trauma, occlusion, and drug induced; however, many cases remain idiopathic. Predisposing factors include an altered immune status, prior skin injury, staphylococcal carrier status, malnutrition, diabetes, obesity, occlusion with topical product use, use of certain medications (topical and systemic steroids, lithium, contraceptive agents, testosterone, danazol, stanozolol, antiepileptics, ethionamide, isoniazid, rifampicin, cyclosporin, epidermal growth factor receptor inhibitors, and long-term use of antibiotics), poorly chlorinated hot tubs, and actinic damage.^{[3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29]}

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Epidemiology

Frequency

Superficial folliculitis is common, but because it is often self-limited and patients rarely present to the doctor; therefore, the exact incidence is unknown. Those who are seen, more often have either recurrent or persistent superficial folliculitis or deep folliculitis. Although the incidence is unknown, conditions that make patients more susceptible include frequent shaving, immunosuppression, preexisting dermatoses, long-term antibiotic use, occlusive clothing and/or occlusive dressings, exposure to hot humid temperatures, diabetes mellitus, obesity, and use of EGF-R inhibitor medications.

Folliculitis has also been reported following smallpox or anthrax vaccine. These cases are more common in military troops who are vaccinated prior to being deployed.^[10]

The acneiform eruption attributed to epidermal growth factor receptor inhibitors occurs in 50-100% of patients and is a dose-dependent drug reaction.^{[6, 7, 8, 9]}

Race

Folliculitis occurs in persons of any race, but pseudofolliculitis and traction folliculitis occurs more commonly in African Americans, whereas classic eosinophilic folliculitis is more common in Japanese persons.^{[5, 11, 12, 28]}

Sex

Although most cases of folliculitis show no sex predilection, folliculitis barbae, folliculitis keloidalis nuchae, perifolliculitis capitis abscedens et suffodiens, and eosinophilic folliculitis occur more frequently in males, whereas traction folliculitis occurs more frequently in females.^{[5, 11, 12, 26, 28, 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.^{[25, 31]}

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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.

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.^{[8, 9]}

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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, 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. 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. 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]

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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.^{[13, 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,^[14] 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]

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.^[15]

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.^[16]

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

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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.^[31] 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.^[25]

An unusual cause of folliculitis occurs as a result of either overgrowth of Demodex mites or an acquired hypersensitivity to the mite. This form of folliculitis manifests with a more diffuse background erythema, in addition to the follicular-centered papules and pustules.^{[17, 29]} This is most commonly seen in immunosuppressed patients.

An uncommon form of folliculitis is due to an infection with herpes viruses. 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.^{[18, 19]}

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.^[20] In contrast to the characteristic lesions seen in most herpes infections, vesicles typically do not occur. Biopsy is often required to confirm the diagnosis.^[19]

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.^[28] 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.

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.^[26]

Acute generalized exanthematous pustulosis and anticonvulsant hypersensitivity syndrome both manifest as an acute onset of a discrete pustular eruption arising shortly after beginning therapy with various medications. Although the eruption that occurs in acute generalized exanthematous pustulosis is often differentiated from anticonvulsant hypersensitivity syndrome by having nonfollicular-based pustules, either condition can have follicular or nonfollicular-based pustules.

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.^{[6, 7, 21]} 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.^[5] 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.^[12]

A second form of eosinophilic folliculitis arises in patients with AIDS and other conditions that result in immunosuppression.^[22] 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.^[3] Eosinophilic folliculitis may also occur after antiretroviral therapy, possibly through macrophage activation.^[4]

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.

In 2010, a report described hypertrophic scars from surgical staples that mimicked folliculitis.^[23]

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Complications

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

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Laboratory Studies

Laboratory studies are typically not obtained because diagnosis is usually made based on history and physical examination findings alone. In cases resistant to standard therapy, cultures, Gram stain, potassium chloride (KOH) preparation, and biopsy are the diagnostic tests of choice.

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 biopsy assists in the identification of folliculitis caused by herpes simplex virus.

A small punch biopsy (3-4 mm) of an active lesion should be performed in atypical cases or in patients resistant to standard treatments.

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

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Procedures

For deep infections, incision and drainage can be therapeutic and can provide material to be sent for culture.

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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.^[32] Note the image below.

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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.

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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.^[18]

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.^[32]

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.^[12]

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.^[7]

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Medical Care

Before a treatment plan is devised, it is important to consider the etiology of the folliculitis, severity, and distribution of the lesions. For uncomplicated superficial folliculitis, use of antibacterial soaps and good hand-washing techniques may be all that is needed. Lesions that are more inflamed usually respond well to warm compresses with or without the use of a topical antimicrobial agent. For refractory or deep lesions with a suspected infectious etiology, 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:

• Pseudomonas folliculitis is usually self-limited and does not require treatment; however, if the patient is immunocompromised or the lesions are persistent, oral ciprofloxacin may be given.
• Eosinophilic pustular folliculitis (Ofuji disease) does not respond to systemic antibiotics. First line treatment is indomethacin (50 mg/day). Other therapies include UVB phototherapy, minocycline, or dapsone.^[24]
• Pityrosporum folliculitis initially responds to topical antifungals such as ketoconazole cream or shampoo but is often associated with relapses. For relapses, systemic antifungals should be tried.
• Gram-negative folliculitis that arises as a complication of chronic antibiotic use is best approached by discontinuing the implicated antibiotic and administering oral trimethoprim-sulfamethoxazole. Use of benzoyl peroxide washes may also be beneficial.
• Herpetic folliculitis responds to valacyclovir, famciclovir, or acyclovir.
• Papulopustular eruption associated with epidermal growth factor receptor inhibitors is self-limited and resolves with cessation of chemotherapy. In patients requiring treatment, topical antibiotics, topical corticosteroids or oral antibiotics, particularly tetracyclines, can be administered.

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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.

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Diet

Because folliculitis is more common in individuals who are obese, weight reduction may be helpful.

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Activity

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.

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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.

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.

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.

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Long-Term Monitoring

Arrange a follow-up visit within 2 weeks to check response to treatment.

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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.

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

• Dosing, Interactions, etc.

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.

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Mupirocin (Bactroban, Centany)

• Dosing, Interactions, etc.

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

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Cephalexin (Keflex)

• Dosing, Interactions, etc.

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.

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Dicloxacillin

• Dosing, Interactions, etc.

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.

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Erythromycin topical (Akne-mycin, Ery)

• Dosing, Interactions, etc.

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.

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Minocycline (Minocin, Dynacin, Solodyn)

• Dosing, Interactions, etc.

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.

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Rifampin (Rifadin)

• Dosing, Interactions, etc.

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.

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Ciprofloxacin (Cipro)

• Dosing, Interactions, etc.

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

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

• Dosing, Interactions, etc.

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.

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Linezolid (Zyvox)

• Dosing, Interactions, etc.

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

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Dapsone (Aczone)

• Dosing, Interactions, etc.

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.

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Class Summary

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

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Indomethacin (Indocin)

• Dosing, Interactions, etc.

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).

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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.

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Ciclopirox (Loprox)

• Dosing, Interactions, etc.

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

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Econazole topical (Ecoza)

• Dosing, Interactions, etc.

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.

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Ketoconazole (Nizoral, Xolegel, Extina)

• Dosing, Interactions, etc.

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.

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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.

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Famciclovir (Famvir)

• Dosing, Interactions, etc.

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

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Valacyclovir (Valtrex)

• Dosing, Interactions, etc.

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.

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Acyclovir (AHydrocort, Alphosyl, Aquacort)

• Dosing, Interactions, etc.

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.

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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.

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