Am J Clin Dermatol 2004; 5 (5): 301-310

THERAPY IN PRACTICE 1175-0561/04/0005-0301/$31.00/0

© 2004 Adis Data Information BV. All rights reserved.

Folliculitis
Recognition and Management
Jesús Luelmo-Aguilar and Mireia Sàbat Santandreu
Unity of Dermatology, Hospital of Sabadell, Sabadell, Spain

Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301
1. Clinical Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301
2. Laboratory Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302
3. Clinical Presentation and Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302
3.1 Infectious Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302
3.1.1 Bacterial Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302
3.1.2 Syphilitic Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
3.1.3 Fungal Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
3.1.4 Viral Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
3.1.5 Parasitic Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
3.2 Non-Infectious Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
3.2.1 Folliculitis of Known Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
3.2.2 Folliculitis of Uncertain Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
3.2.3 Folliculitis Associated with HIV Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
3.2.4 Skin Disorders with Follicular Expression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
3.3 Pseudofolliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308

Abstract Folliculitis is an inflammatory reaction in the superficial aspect of the hair follicle and can involve the
follicular opening or the perifollicular hair follicles. The pilosebaceous unit of the follicle is divided into three
compartments: the infundibulum (superficial part, outlined by the sebaceous duct), the isthmus (between the
sebaceous duct and arrector pili protuberance), and the inferior segment (stem and hair bulb). This anatomical
scheme forms the basis for any evaluation of the clinical manifestations of folliculitis. Most of the follicular
conditions can be classified according to their anatomical location and histopathologic patterns. Clinically, the
inflammation manifests as 1mm-wide vesicles, pustules, or papulopustules in acute cases; however, hyperkera-
tosis and keratotic plug formations are indicative of a chronic process. The presence of superficial pustules does
not always imply an infectious origin, as there are many noninfectious types of folliculitis.
In this review, we describe the different types of folliculitis based on their etiology, clinical manifestation,
and treatment. We also discuss some newly described disorders and the latest information on their treatment.

Folliculitis is an inflammatory reaction in the superficial aspect
of the hair follicle and can involve the follicular opening or the
perifollicular hair follicles. The pilosebaceous unit of the follicle is
divided into three compartments: the infundibulum (superficial
part, outlined by the sebaceous duct), the isthmus (between the
sebaceous duct and arrector pili protuberance), and the inferior
segment (stem and hair bulb). This anatomical scheme forms the
basis for any evaluation of the clinical manifestations of follicu-
litis.
1. Clinical Evaluation
Clinical information is very useful in recognizing the causes of
folliculitis. Pruritus is the most frequent symptom, as is common
in other inflammatory skin dermatoses. A detailed history is
needed to determine the etiology.[1] It is very important to question
302
Is there a predisposing factor to cutaneous infection?
Yes No
Swab of the lesions Ask about :
PCR Job
Serology HIV Drug intake
Serology hepatitis virus Exposure to heated water
Serology syphilis Exposure to contaminated water
Other dermatitis
No No
Confirm infection Histopathologic study
or relationship Confirm folliculitis
Fig. 1. Algorithm for the clinical evaluation of folliculitis. PCR = polymerase
chain reaction.
the patient about predisposing factors to cutaneous infections,
including: drug abuse; an underlying immune deficiency; expo-
sure to possibly contaminated heated water (hot tub, spa bath,
heated swimming pool, or bath water); and exposure to kittens,
guinea pigs, or farms. It is also important to know the patient’s
age, sex, race, job, and the possibility of other associated dermati-
tis. A physical examination usually shows the highly characteristic
elementary lesions formed by follicular and perifollicular pustules,
papules, and papulopustules, but in some cases there is a predomi-
nance of papules or keratotic plugs. Noting the location and
distribution of the lesions is very helpful, as is knowledge of their
evolution. An algorithm for the clinical evaluation of folliculitis is
given in figure 1.
2. Laboratory Investigation
Swabs and Gram stains of the pustule content should be rou-
tinely collected to exclude a diagnosis of bacterial or viral follicu-
litis. Scrapings should also be taken for fungal culture. A potassi-
um hydroxide preparation may identify a yeast form or candida. In
addition, a Tzanck smear is useful in cases of herpetic viral
folliculitis. If a predisposing factor exists, or clinical suspicion,
serological tests for HIV or syphilis can be done. In some cases of
viral folliculitis, the diagnosis can be confirmed by polymerase
chain reaction (PCR). Histopathologic studies enable a correct
classification and diagnosis if the patient so requires.
3. Clinical Presentation and Management
3.1 Infectious Folliculitis
3.1.1 Bacterial Folliculitis
Bacterial folliculitis may be superficial or deep. Superficial
folliculitis (Bockhart impetigo) consists of small pustules, often
surrounded by a ring of erythema located within follicular orifices.
The pustules develop in clusters and form crusts during the evolu-
© 2004 Adis Data Information BV. All rights reserved.
Luelmo-Aguilar & Sàbat Santandreu
tion of the folliculitis, often involving the face, buttocks, and
axillae in infants and children; the legs in adolescent girls; and the
flexural areas in adolescent boys. The pustules usually heal in a
few days but occasionally develop into furuncles.
Bacterial folliculitis usually occurs in children or adults with a
predisposing factor that helps to increase the number of bacteria on
the surface of the skin (table I). Staphylococcus aureus is the most
frequent causative agent,[2,3] and species of Streptococcus, Pseu-
domonas, Proteus, and coliform bacteria have also been implicat-
ed in the infection.[4,5] Pseudomonal folliculitis involves the ex-
posed aspects of the trunk and follows an exposure to contamina-
ted water (figure 2).
Furuncles occur as a result of the spread of bacterial infection
into the tissues of the follicle, beneath the infundibulum, either at
the onset of infection or during the evolution of superficial follicu-
litus. A furuncle begins as a small, painful follicular inflammatory
nodule that becomes pustular and in few days develops central
necrosis, and heals after a discharge of necrotic material, leaving a
permanent scar (figure 3). Staphylococci are the most common
causative organism, including S. epidermidis, and streptococci and
coliform bacteria have also implicated in some cases. Furuncles
are more common in young adults, especially boys, and the most
affected areas are the face, back of the neck, breasts, axillae,
perineum, buttocks, and thighs. Predisposing factors for the devel-
opment of furunculosis include: chronic staphylococcal carriers,
diabetes mellitus, malnutrition, and HIV infection.
Bacterial sycosis is a subacute or chronic staphylococcal infec-
tion that involves the entire hair follicle. The condition occurs in
males after puberty, most frequently in the third and fourth de-
cades of life. The lesions begin with an edematous, inflammatory
follicular papule or pustule located in the beard (usually on the
upper lip), accompanied by a burning sensation. In a few days
numerous pustules develop, involving the neighboring follicles,
that may coalesce to produce plaques studded with pustules. The
chronic form may persist for years and in some severe cases
(lupoid sycosis) the follicles are destroyed by scarring.[2,3]
Table I. Factors predisposing bacterial folliculitis
Nasal carriage of Staphylococcus aureus
Occlusion
Maceration
Hyperhydration
Complicating pruritic skin diseases (e.g. scabies, eczemas)
Vigorous application of topical medications (corticosteroids)
Shaving against the direction of hair growth (folliculitis on leg)
Exposure to oils and certain chemicals
Pin worm infestation (folliculitis of buttocks)
Exposure to heated water (hot tub, heated swimming pool) or
contaminated water
Am J Clin Dermatol 2004; 5 (5)
Recognition and Management of Folliculitis
Fig. 2. Pseudomonas folliculitis: inflammatory pruriginous papulopustulous
rash, localized on the chest.
Superficial bacterial folliculitis usually responds to treatment
with topical antibacterials such as mupirocin or fusidic acid oint-
ment. Gram negative folliculitis needs to be identified and elimi-
nated from the source of the infection. Although superficial bacter-
ial folliculitis often resolves spontaneously, some patients require
oral antibacterial treatment, such as ciprofloxacin (table II).
To eradicate skin colonization in Bockhart impetigo (superfi-
cial folliculitis) caused by staphylococcal infection the patient
should be advised to take a 5-minute daily bath with Oilatum® 1, a
liquid paraffin compound with moisturizing and antiseptic proper-
ties, plus bath oil in the bath water for a minimum of 4 weeks. In
addition, to eradicate clothing contamination, clothing, linen, and
towels should be routinely washed in hot water. Finally, predis-
posing factors need to be identified and eliminated.
In cases of deep bacterial folliculitis, an appropriate oral anti-
bacterial, based on the results of the culture, is mandatory.[6]
Incision and drainage may sometimes also be necessary.
3.1.2 Syphilitic Folliculitis
Secondary syphilis is characterized by various types of cutane-
ous lesions. Pustulous syphilis is infrequent and the lesions may
present as a pustulous, papulo-pustulous, or papule-crust rash
without fever. Acneiform syphilis is a form of granulomatous
perifolliculitis in late syphilis with circinate papular-nodular le-
sions. The diagnosis of this infection requires an accurate history
and strong clinical suspicions.[7]
3.1.3 Fungal Folliculitis
Superficial mycoses are very common. They are divided into
three groups: dermatophytic, pityrosporum, and candida follicu-
litis.
1 The use of trade names is for product identification purposes only and does not imply endorsement.
© 2004 Adis Data Information BV. All rights reserved.
303
Dermatophytic Folliculitis
Dermatophytic folliculitis is usually caused by a zoophilic
species and can produce different types of clinical manifestation
according to the infected body area, including: tinea capitis, tinea
barbae, tinea corporis, tinea cruris, and tinea pedis.[8] This condi-
tion presents clinically as follicular pustules surmounting an indu-
rated erythematous plaque with peripheral extension. Hair shaft
loss is typical and depends on the degree of inflammation, which
relates to the depth of penetration.
The most important form of dermatophytic folliculitis is tinea
capitis, which mainly affects children and has four variants: (i)
noninflammatory; (ii) ‘black dot’; (iii) favus; and (iv) kerion. The
first two forms are usually nonscarring with minimal inflamma-
tion, whereas the latter two involve severe suppurative and granu-
lomatous folliculitis and permanent hair loss.
When treating tinea capitis, topical antifungals are not effec-
tive. Nevertheless, to decrease sporax spread, an antifungal sham-
poo can be used (table II). In children, griseofulvin (10–20 mg/kg/
day) for a minimum of 6 weeks remains one of the first steps in
treatment. Good results have been achieved with terbinafine (125
mg/day, 6 weeks).
Trichophytic granuloma (Majocchi granuloma) is a classical
type of inflammatory tinea corporis located on the legs with
perifollicular granulomatous papules, primarily caused by
Trichophyton rubrum.[9]
Tinea barbae is a disease that mainly affects adult males,
usually in the beard and moustache areas. Infections caused by
zoophilic species are responsible for the great majority of cases;
the two main species involved are T. mentagrophytes and T.
verrucosum. Clinically, tinea barbae displays deep folliculitis with
red inflammatory papules and pustules and exudation or crusting.
Hair shaft loss is also present (figure 4).
Kerion and favus are both deep suppurative types of folliculitis
infecting the scalp, which are usually complicated by pain, fever,
Fig. 3. Recurrent furunculosis in an immunosuppressed woman.
Am J Clin Dermatol 2004; 5 (5)
304 Luelmo-Aguilar & Sàbat Santandreu

Table II. Treatment of infectious folliculitis 3.1.4 Viral Folliculitis

Type of folliculitis Topical Systemic Folliculitis due to herpes simplex virus (HSV) and molluscum
Staphylococcal Fusidic acid or mupirocin Dicloxacillin, flucloxacillin, contagiosum is a rare condition and might be considered a sign of
and streptococcal ointment (tid) fusidic acid, azithromycin immunosuppression, especially in cases caused by molluscum
Gram-negative Dilute acid acetic baths Ciprofloxacin contagiosum.[13-15] The clinical presentation in HSV-induced fol-
bacteria
liculitis involves pruritic multiple erythematous papules or
(pseudomonas)a
papulovesicles with crusts or umbilicated vesicles on the face.
Dermatophytes Antifungal shampoo Griseofulvin, terbinafine,
itraconazole
Molluscum contagiosum folliculitis presents as multiple discrete
pruritic whitish papules over the beard area. Frequently, patients
Pityrosporum Topical azoles,
shampoos with sulfur of with herpetic folliculitis have a history of recurrent herpes infec-
selenium tions on the face. Further investigation is mandatory, especially in
Candidal Itraconazole cases of molluscum contagiosum folliculitis that occurs in immu-
Herpetic Aciclovir, valaciclovir, nocompetent subjects, or that may be a sign of underlying immune
antihistamines deficiency, such as HIV infection. There are several some reports
Molluscum (pox Curettage, cryotherapy, of folliculitis caused by herpes zoster infection.[16]
virus) cantharidin,
In viral herpetic folliculitis, the recommended treatment is oral
podophyllotoxin,
trichloroacetic acid. antihistamines or aciclovir 200mg five times daily for 5 days.[13]
Demodicidosis 5% permethrin cream Itraconazole, ivermectin
There are different modalities to treat molluscum contagiosum
a Usually resolves spontaneously. folliculitis, the most common is cutterage (table II).
tid = three times daily.
3.1.5 Parasitic Folliculitis

and regional lymphadenopathy that results in scarring and perma- Demodex spp. mites normally inhabit the hair follicles and
nent hair loss. Kerion is caused predominantly by Microsporum sebaceous glands. Only D. folliculorum and D. brevis are found in
canis and T. verrucosum, and favus, the more severe form, is humans, both in sebaceous areas such as the chest, back, temple,
caused by T. schoenleinii (figure 5). periorbital area, and nose. D. folliculorum has been implicated in
many dermatitides characterized by the presence of numerous
In these cases oral therapy is essential (griseofulvin, terbina-
mites, such as rosacea-like eruptions on the face, perioral dermati-
fine).
tis, pityriasis folliculorum, blepharitis, eosinophilic pustular fol-
liculitis, and papular lesions associated with AIDS (figure 6).
Pityrosporum Folliculitis
Typically, all of these dermatoses respond rapidly to appropriate
Pityrosporum folliculitis is caused by pityrosporum yeasts, therapy with 5% permethrin cream (topical) or itraconazole or
most commonly Pityrosporum orbiculare. The condition mainly ivermectin (systemic). [17-19]
affects teenagers and men, probably as a result of the production of
free fatty acids by the yeast and blockage of the follicular ostium
by scale.[10] The lesions are erythematous follicular papules and
pustules located on the back, upper trunk, and shoulders, and are
frequently pruritic. Treatment with a topical antifungal is usually
effective (table II).[11]

Candida albicans

Pustular folliculitis caused by Candida albicans is a rare condi-

tion reported in individuals who abuse heroin; the condition in-
volves candidemia, leading to pustules and nodules in the hair-
bearing areas. Pustular folliculitis has also been reported in healthy
individuals, with widely distributed and painful pustules.[12]
Candidal folliculitis must be treated with oral itraconazole (200 Fig. 4. Tinea barbae: typical location on the moustache, with hair loss and
mg/day). high inflammatory response.

© 2004 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2004; 5 (5)
Recognition and Management of Folliculitis 305

Folliculitis Caused by Nutritional Deficiencies

Severe vitamin C deficiency causes scurvy. It requires about 2
months of deprivation to produce mucocutaneous signs, including:
perifollicular petechiae, follicular hyperkeratosis, gingival hemor-
rhage, and hyperplasia. The follicular eruption occurs on the
lowers legs, anterior forearms, and abdomen.[25]
One of the earliest signs of vitamin A deficiency is night
blindness. The skin shows follicular hyperkeratosis, dryness, and
generalized wrinkling.[26]

Actinic Superficial Folliculitis

Actinic folliculitis was described in 1985 in young adults of
Fig. 5. Favus: crust, exudation, and pustulation with hair loss on a young both sexes.[27] It always occurs within 24–48 hours of sun exposure
boy’s head.
and is characterized by numerous sterile follicular pustules on the
shoulders, trunk, and arms, accompanied by a burning sensation. It
3.2 Non-Infectious Folliculitis usually resolves within 10 days. Sunscreens provide partial protec-
tion.[28]
3.2.1 Folliculitis of Known Etiology
3.2.2 Folliculitis of Uncertain Etiology

Acneiform Folliculitis
Acne Vulgaris
Acneiform folliculitis is frequently drug induced. The use of
Acne is one of the most prevalent dermatoses in adolescents,
systemic and topical corticosteroids and corticotropin can result in
and involves the face and upper trunk. The origin of the acne
follicular skin eruptions consisting of small and inflammatory
lesions is an alteration, with or without inflammation, in the
pustules distributed over the face, chest, shoulders, neck and upper
follicular apparatus that forms comedones, papules, pustules, nod-
back. Lithium typically produces an acneiform eruption and fol-
ules, or cysts.
liculitis in the same areas as acne vulgaris, or it may be more
Acne vulgaris has many different modalities of treatment.
extensive; the condition begins within days of starting lithium
Topical antibacterial treatment is now recommended less than it
treatment, may be pruritic, and resolves quickly with discontinua-
used to be, and only for short periods, to avoid the development of
tion. Halogens such as bromides and iodides that are administered
resistances. The combination of topical retinoids, particularly
systemically may produce an acneiform eruption similar to corti-
adapalene (a retinoid-like agent), with topical antibacterials or
costeroid-induced acne but more extensive and inflammatory.
azelaic acid is one of the most efficacious therapies.[29] Oral
Tuberculostatic drugs such as isoniazid and rifampin (rifampicin)
therapy options include different antibacterials (minocycline,
can produce acneiform eruptions.[20-23]
doxycycline), isotretinoin, and oral contraceptives.[30]
Occupational acne appears after exposure to cutting oil,
dichlorodiphenyltrichloroethane (DDT), halogenated hydrocar-
bons, crude coal tars, asbestos, and heavy destilated water. The
eruption consists of inflammatory pustules, papules, comedones,
and nodules, located on covered areas such as the buttocks, thighs,
and forearms. Exposure to chlorinated aromatic hydrocarbons
produces an acneiform skin reaction called chloracne, character-
ized by open and closed comedones with many inflammatory cysts
located on the face (malar eminences, temples, postauricular areas,
and neck).
In cases of folliculitis with known etiology, the treatment is
obvious: avoid the cause and correct the possible deficiencies.
Anti-acne topical therapies are sometimes needed. Some ac-
neiform dermatoses, especially those induced by drugs, respond Fig. 6. Demodex folliculitis: excoriated papules on the face of a child with
well to topical tretinoin (vitamin A acid) treatment.[24] atopic dermatitis.

© 2004 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2004; 5 (5)
306 Luelmo-Aguilar & Sàbat Santandreu

Table III. Treatment of folliculitis of uncertain etiology

Type of folliculitis
Acne keloidalis
Folliculitis decalvans
Rosacea
Perioral dermatitis
Fox-Fordyce disease
Idiopathic follicular mucinosis
Perforating folliculitis
Disseminate and recurrent
infundibulofolliculitis
Eosinophilic pustular folliculitis
Topical
Potent corticosteroid
(fluocinonide)
Mupirocin
1% metronidazole, 20% azelaic
acid cream, retinoid
1% metronidazole
Clindamycin solution
Corticosteroid, tacrolimus
Systemic
Oral antibacterial (tetracycline)
Rifampin (rifampicin) + clindamycin,
fusidic acid, tyrosine (L-tyrosine),
zinc
Metronidazole, minocycline,
doxycycline, clarithromycin,
isotretinoin
Tetracycline, erythromycin
Oral retinoids, surgery
Phototherapy, minocycline
Allopurinol
Isotretinoin
Naproxen, cetirizine, corticosteroid
Comment
In combination; long term
In combination; long term
Eradicate Helicobacter pylori; or
Demodex folliculorum infection;
tacrolimus for corticosteroid-induced
rosacea
Discontinue topical corticosteroid
Usually self-limited
Spontaneous resolution

Keloidal Folliculitis (Acne Keloidalis Nuchae) Rosacea

Keloidal folliculitis or acne keloidalis nuchae is a chronic,
scarring folliculitis that mostly affects Black patients. The lesions
are located on the back of the neck and the occipital scalp. It begins
as small, firm papules and occasional pustules that progress to
keloidal papules and plaques and progressively lead to hyper-
trophic scars, chronic abscesses, and hair loss. The cause remains
unknown and can be multifactorial.[31] Keloidal folliculitis has
been associated with seborrheic dermatitis, acne vulgaris, and
tufted hair folliculitis.[31,32]
At present there is no appropriate therapy for acne keloidalis.
Some authors recommend a combination of a potent topical corti-
costeroid with prolonged use of an oral antibacterial, such as
tetracycline (table III).[31] Treatment of folliculitis decalvans is
also very difficult. There are reports demonstrating a good res-
ponse to oral fusidic acid and zinc treatment.[33] Anecdotal reports
suggest that shaving the scalp may be a successful strategy.[34] The
best treatment seems to be an early course of rifampin combined
with clindamycin.[35] It is not advisable to use rifampin alone, due
to the rapid emergence of staphylococcal resistance.
Folliculitis Decalvans
Folliculitis decalvans is characterized clinically by chronic
folliculitis that leads to progressive scarring and alopecia. It may
involve the scalp alone or together with any other hairy regions. It
initially presents as crops of follicular pustules, followed by de-
struction of the hair shaft and slow progression of the alopecia.
Some recent reports suggest the possibility of a genetic predisposi-
tion.[36] S. aureus infections seem to play an important role in the
pathogenesis of this anomaly.[35]
Rosacea is a common condition of unknown etiology. Many
possible causes have been described such as genetic predisposi-
tion, Helicobacter pylori infection, and D. folliculorum infestation
among others. It occurs in middle-aged men and women as a result
of an inflammation within and around follicular infundibula. The
lesions consist of papules, pustules, and telangiectasia that affect
the face and nose.
Most cases of rosacea respond well to long-term topical anti-
bacterial treatment, such as 1% metronidazole or 20% azelaic acid
cream (table III). Oral or topical retinoids may also be effective.
Systemic treatment options for rosacea include metronidazole,
minocycline, doxycycline, clarithromycin, and isotretinoin.[37]
Many authors recommend the eradication treatment of H. pylo-
ri,[38] while others recommend 10% crotamiton, 5% permethrin,
and oral or topical ivermectin to treat D. folliculorum infec-
tion.[39,40] Tacrolimus can be useful in corticosteroid-induced
rosacea.[41]
Perioral Dermatitis
Perioral dermatitis is most frequent in childhood and in young
women. Its exact origin is not known. Skin lesions consist of flesh-
colored or inflamed papules, micronodules, and pustules with
variable pruritus. The condition is probably a localized form of
rosacea with the same clinical lesions but restricted to the perioral
region and lower eyelids. The only clearly associated factor with
this condition is the use of fluorinated topical corticosteroids.
Greasy cosmetics and hyperandrogenemia are also implicated in
the etiology of perioral dermatitis.
Treatment of perioral dermatitis consists of discontinuing topi-
cal fluorinated corticosteroid use, if any, and using topical metro-

© 2004 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2004; 5 (5)
Recognition and Management of Folliculitis
nidazole alone or in combination with either oral tetracycline or
erythromycin (table III).[42] Successful treatment with topical
adapalene has also been reported recently.[43]
Fox-Fordyce Disease
Fox-Fordyce disease is a chronic condition involving itchy,
rounded, follicular papules localized to the areas of the skin
containing apocrine sweat glands, such as axillae, pubes, areolae,
and periumbilical and presternal areas. This distribution of skin
changes suggests an apocrine origin, affecting the follicular infun-
dibulum at the site of entry of the apocrine duct. It is nine times
more frequent in women than men and occurs between the ages of
13 and 35 years.[44]
Fox-Fordyce disease has been successfully treated with a topi-
cal clindamycin solution, with oral retinoids, and with surgery
(table III).[45-47]
Pruritic Folliculitis of Pregnancy
Pruritic folliculitis of pregnancy (PFP) was first described in
1981.[48] PFP is a generalized pruritic, erythematous, papular
eruption occurring in pregnant women. Some authors suggest that
PFP should be included under the polymorphic eruption of preg-
nancy.[49] Pathologic features of the condition correspond to sterile
folliculitis, but the etiology is unknown. No morbidity to the
mother or fetus has been observed, and the eruption was found to
clear spontaneously in the postpartum period.[50]
Eosinophilic Pustular Folliculitis
Eosinophilic pustular folliculitis (EPF) was first described by
Ofuji et al. in 1970 in three Japanese patients.[51] However, the
etiology is uncertain. There are three different variants: classic
EPF or Ofuji disease; EPF associated with HIV infection; and the
infantile form of EPF.
The classic form is characterized by recurrent outbreaks of
follicular erythematous papules and pustules that may coalesce to
form polycyclic plaques, with central healing and peripheral ex-
tension. It is often pruritic and usually involves seborrheic distri-
bution, but may also be found in 20% of patients on the trunk,
proximal extremities, palms, and soles of the feet.[52]
EPF associated with HIV infection is often different from the
classic form and may include erythematous non-follicular papules,
urticariform lesions, large erythematous plaques, or even a genera-
lized rash. The face, trunk, and extremities can be affected, but not
the palms and soles (figure 7). This variant is usually chronic and
persistent. It is always very pruriginous and often heavily excoriat-
ed.[53-55]
Infantile EPF presents as numerous sterile pustules located on
>90% on the scalp, although it can also affect the trunk, face, and
extremities. It usually begins in the neonatal period.[56-58]
The histologic image of EPF, with the pilosebaceous structure
infiltrated by a mixture of eosinophils and neutrophils, is not seen
in any other entity.[59]
© 2004 Adis Data Information BV. All rights reserved.
307
Eosinophilic pustular folliculitis has many treatments, includ-
ing naproxen, topical and oral corticosteroids, and cetirizine (table
III).[55-57] Some recent cases not associated with HIV infection
have been reported; these were treated with tacrolimus ointment
with good results.[60] Spontaneous resolution can occur. In cases of
EPF associated with HIV infection, as with most of the other HIV-
associated dermatoses, the best treatment seems to be combination
therapy and the restoration immunity.[36,55]
Toxic Erythema of the Newborn
Toxic erythema of the newborn represents a benign, self-
limiting pustular eruption of the neonatal period of unknown
etiology. The rash is composed of erythematous macules, papules,
pustules, or a combination of these elements. Lesions may occur
anywhere and appear during the first 3–4 days of life and fade
during the following 2 week period. No therapy is indicated.[61,62]
Follicular Mucinosis
Follicular mucinosis or alopecia mucinosa is an inflammatory
disorder characterized clinically by follicular papules and more or
less indurate plaques. The face and neck are most commonly
involved. It can be classified into two groups. The first type is the
most common and benign form; in younger patients it is often
limited to a few lesions on the head and neck, whereas in older
patients it often involves more lesions in a more generalized
distribution. Lesions spontaneously resolve within 2 years. The
second type, which presents in elderly patients as disseminated
plaques, coexists with a malignant lymphoma, especially mycosis
fungoides.[63,64]
The idiopathic form of follicular mucinosis has been treated
with phototherapy and minocycline (table III).[65,66] In addition,
there are some cases of acquired reactive perforating dermatoses
successfully treated with allopurinol.[67]
Fig. 7. Eosinophilic pustulous folliculitis in an HIV-infected man with ery-
thematous, inflammatory papules, and some urticarial lesions.
Am J Clin Dermatol 2004; 5 (5)
308
Perforating Folliculitis
Included among the perforating disorders, perforating follicu-
litis is more frequent in women and may persist for many years. It
presents as an asymptomatic eruption of small follicular keratotic
papules on the buttocks and the extensor surfaces of the extremi-
ties. There is a relationship with diabetic nephropathy.[68]
Disseminated and Recurrent Infundibulofolliculitis
Disseminated infundibulofolliculitis is an uncommon condition
that occurs mainly in Black patients. Clinically it presents as
multiple disseminated follicular pinpoint papules on the trunk and
limbs, sparing the flexures. Pruritus is often present and the
course is chronic or recurrent and usually unresponsive to local
or systemic treatment; however, some cases will respond to isotre-
tinoin therapy.[69,70]
Disseminated and recurrent infundibulofolliculitis is often self
limited and usually unresponsive to treatment. Occasional re-
sponses to isotretinoin have been described.[69]
3.2.3 Folliculitis Associated with HIV Infection
Immune Recovery Inflammatory Folliculitis
The restoration of immune function with highly active antire-
troviral therapy (HAART) can induce a regression of some skin
problems. However, this restoration against previously
nonpathogenic infectious agents (i.e. D. folliculorum, Pityrospo-
rum spp.) results in recognition of the agent by the immune system
and may lead to the development of immune recovery inflamma-
tory folliculitis in patients with a good immunologic res-
ponse.[71,72] The condition regresses after topical corticosteroid
therapy.
3.2.4 Skin Disorders with Follicular Expression
There are some skin disorders that can produce a follicular
eruption. Atopic dermatitis is one of these diseases and may
present with widely dispersed prominent follicular papules.[73]
A form of psoriasis called follicular psoriasis,[74] which occurs
especially in children, presents as small desquamative follicular
papules located mainly in the upper arms and the extension areas.
This condition may be confused with pityriasis rubra pilaris (fig-
ure 8). There are some unusual reported cases of follicular sar-
coidosis.[75]
3.3 Pseudofolliculitis
Pseudofolliculitis, a chronic inflammatory condition mainly
observed in Black patients,[76,77] is not a true folliculitis. The basis
of its etiology is an inflammatory reaction that occurs after shav-
ing, when the sharp edge of the hair shaft transects the wall of the
hair follicle or re-enters the epidermis. Papules and pustules in the
beard distribution are the most common; however, other affected
areas in predisposed individuals may include the scalp, axillae,
© 2004 Adis Data Information BV. All rights reserved.
Luelmo-Aguilar & Sàbat Santandreu
Fig. 8. Follicular psoriasis on the arm. Note the papulosquamous lesions
with follicular distribution (confirmed by histopathologic study).
pubis, and legs. The most effective treatment seems to be laser hair
removal using longer wavelengths.[78]
4. Conclusions
The term folliculitis is used to describe a superficial inflamma-
tion of the hair follicle. To ascertain the possible causes it is
necessary to have wide clinical information with a complete
physical examination. It is also important to ask about predispos-
ing factors to cutaneous infection. In order to clarify and simplify
the spectrum of folliculitis, we have classified them into infectious
and non-infectious folliculitis categories with clinical and thera-
peutical comments. All the pustular lesions should be cultured
(bacterial, fungal or viral). Complementary studies can also be
done in relation to clinical suspicion (HIV serology, syphilis, PCR
or biopsy).
There are many different types of non-infectious folliculitis,
some of them with known etiology. The knowledge of these
entities allows us to make a correct diagnosis and to provide
specific treatment where possible. It should not be forgotten that
there are skin diseases with follicular expression, such as atopic
dermatitis or psoriasis.
Acknowledgments
No sources of funding were used to assist in the preparation of this review.
The author has no conflicts of interest that are directly relevant to the content
of this review.
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