Etiology
Folliculitis is most commonly infectious in origin. The causative microorganisms include bacteria, fungi, viruses, or Demodex mite.
The most common cause of superficial folliculitis is Staphylococcus aureus.
Gram-negative species implicated include Klebsiella, Enterobacter, and Proteus. These organisms can be seen in acne vulgaris when long-term systemic antibiotic therapy is being given. Pseudomonas aeruginosa, a gram-negative bacteria, causes hot tub folliculitis.
Fungal folliculitis is typically caused by infection with dermatophytes, Malassezia and Candida species; it is often seen in young men on the upper chest and back.
Herpes simplex, Varicella zoster, and Molluscum contagiosum viruses are commonly responsible for viral folliculitis.
Demodex folliculitis is caused by the ectoparasite Demodex folliculorum. Demodex mites are common inhabitants of the skin and pilosebaceous unit.
S aureus and dysfunction of the local immune response may play a role in folliculitis decalvans, an inflammatory scalp disorder.[14][15]
Hidradenitis suppurativa or acne inversa presents with papules, nodules, and scarring in intertriginous skin (axillae, groin, under breasts). It may also present with folliculitis in early/mild cases.[16]
Pathophysiology
Depending on the etiology of folliculitis, different populations of inflammatory cells infiltrate the walls and/or lumens of the hair follicles. In superficial Staphylococcus aureus folliculitis, a predominantly neutrophilic cell population infiltrates the infundibular portion of the hair follicle. In the deeper variant (sycosis), neutrophils extend beneath the infundibulum to form abscesses. When the inflammation is extensive, extension of neutrophils into the perifollicular regions lead to large abscess formations (furuncles and carbuncles).[17]
In fungal folliculitis, a neutrophilic infiltrate is found around the hair follicles. In Majocchi granuloma, a form of fungal folliculitis, hyphal invasion of the cornified keratinocytes of the hair follicle incites a suppurative inflammatory response. This leads to rupture of the hair follicle and the ensuing granulomatous dermal reaction.
In viral folliculitis, caused by Herpes simplex, Varicella zoster, or Molluscum contagiosum, a dense, perifollicular lymphohistiocytic infiltrate is seen on histology. In comparison, mites can be appreciated on histology in patients with Demodex folliculitis.
Similar to S aureus folliculitis, folliculitis decalvans involves a neutrophilic infiltrate. However, the neutrophilic infiltrate of folliculitis decalvans extends beyond the infundibular portion of the follicle and involves the deep intrafollicular and perifollicular regions.
Recurrent and chronic folliculitis can ultimately lead to the destruction of the hair follicle and scarring.
Classification
Folliculitis subtypes
Staphylococcus aureus
This condition can be either superficial (follicular impetigo of Bockhart) or deep (sycosis).
Gram-negative
This typically affects patients with acne treated with oral antibiotics and is associated with Klebsiella, Enterobacter, or Proteus infections. One form of gram-negative folliculitis is termed hot tub folliculitis, which is caused by Pseudomonas aeruginosa following immersion in spa water.
Fungal
This form is caused by infection with dermatophytes, Malassezia, and Candida species; it is often seen in young men on the upper chest and back.
Viral
Pathogenic viruses include herpes simplex virus, Varicella zoster virus, and Molluscum contagiosum.
Demodex
Demodex folliculitis is caused by Demodex folliculorum.
Eosinophilic pustular (Ofuji disease)
Characterized by recurrent, intensely pruritic papules and pustules that develop in an explosive fashion, typically on the face, back, and arms.[1]
AIDS-associated eosinophilic
This is seen in patients with HIV, usually with a low CD4+ count <300 cells/mm³.[2] Clinically, this condition is characterized by chronic, intensely pruritic, edematous folliculocentric papules involving the upper torso and the head.
Eosinophilic pustular in infancy
This condition presents as pustules and vesicles primarily involving the scalp. The lesions often have an erythematous base and crusting. The condition is self-limiting but can recur in cycles of 3 months to 5 years.[3][4]
Drug-induced acneiform eruptions
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