Folliculitis

Published on 18/03/2015 by admin

Filed under Dermatology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 3669 times

[level-membership-for-dermatology-category]

Folliculitis

Maricarr Pamela M. Lacuesta and Robert G. Phelps

Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports

image

Folliculitis is inflammation of the pilosebaceous follicle. Inflammation limited to the superficial portion of the follicle clinically presents with erythematous papules and pustules, while deeper involvement manifests with furuncles and abscesses. Etiologic factors include both infectious and non-infectious agents.

Bacterial pathogens are the predominant causes of infectious folliculitis. These include Gram-positive Staphylococcus aureus, Micrococcus, Streptococcus pyogenes and Clostridium perfringens, Gram-negative Pseudomonas, Klebsiella, Proteus, Enterobacter and Citrobacter spp., Acinetobacter baumannii and Aeromonas hydrophila, Treponema pallidum and mycobacteria. Herpes and molluscum cause viral folliculitis while Candida spp., Pityrosporum spp., Rhodotorula spp., Trichosporon cutaneum and dermatophytes cause fungal folliculitis. Parasitic folliculitis may be due to Demodex spp., scabies or larva migrans. Definitive diagnosis is achieved by identification of the infectious agent/s; however, thorough history taking and detailed physical examination may provide helpful clues to the diagnosis. For example, atopic patients are particularly susceptible to staphylococcal folliculitis; a lamellar circle of desquamation surrounding the papules or pustules is a valuable clinical finding.

There should be a high index of suspicion for Gram-negative folliculitis in acne patients treated with long term antibiotics. Exposure to contaminated water in pools or jacuzzis can lead to folliculitis by Pseudomonas aeruginosa or Aeromonas hydrophila. Candida folliculitis is a frequent finding in individuals with heroin addiction and one form may preferentially affect the male beard area. Pityrosporum folliculitis, favoring the upper trunk, is more commonly found in regions with hot and humid climate and has recently been reported in a Crohn disease patient treated with infliximab. Demodex folliculitis is suggested by rosacea-like lesions on the face with periorificial accentuation. This is common among young pubescent patients but may also be associated with HIV infection or leukemia. Immunocompromised patients, most notably with HIV infection, develop not only widespread folliculocentric lesions caused by bacteria, viruses or parasites but also a characteristic sterile eosinophilic pustular folliculitis which is paradoxically related to both immune suppression and reconstitution. The clinician should utilize laboratory examinations that aid in the isolation of the infectious agents.

Non-infectious folliculitis may be associated with mechanical factors (friction, occlusion or follicular trauma), of which epilation is an example. Folliculitis has also been reported to develop over the recipient area after hair transplantation. Coal tar and cutting oils cause irritant folliculitis while sun exposure causes actinic folliculitis. Other associations include rheumatologic disorders (Behçet disease, Reiter syndrome, systemic lupus erythematosus, mixed connective tissue disease, and rheumatoid arthritis), inflammatory bowel disease, blood dyscrasias, and pregnancy. Perforating folliculitis is not only associated with diabetes mellitus and renal failure but also with TNF-α inhibitors (infliximab). The etiopathogenic mechanism for necrotizing infundibular crystalline folliculitis (waxy papules with folliculocentric filamentous birefringent crystalline deposits) is hypothesized to be physical/chemical injury or yeast and bacterial action.

Agents responsible for drug-induced folliculitis include epidermal growth factor receptor (EGFR) inhibitors, TNF-α inhibitors, trastuzumab, sorafenib, lapatinib, lenalidomide, lithium, halogens, anti-tuberculous medications, and corticosteroids.

First-line therapies

Topical therapy  
imageFusidic acid or mupirocin for Staphylococcus aureus A
imageRetapamulin for Staphylococcus aureus B
imageMupirocin for eradication of S. aureus colonization of the nares; tea tree oil soap or body wash for body B
imagePovidone-iodine, acetic acid or gentamicin for P. aeruginosa A
imagePermethrin cream for Demodex spp. D
imageMetronidazole cream or gel for Demodex spp. D
imageCorticosteroid for eosinophilic pustular folliculitis C
imageTacrolimus for eosinophilic pustular folliculitis D
Oral therapy  
imageCo-trimoxazole, clindamycin, doxycycline, fusidic acid for Staphylococcus spp. B
imageCiprofloxacin for Pseudomonas folliculitis C
imageItraconazole for Pityrosporum spp. C
imageIvermectin or metronidazole for Demodex spp. D
imageIndometacin or cyclosporine for eosinophilic pustular folliculitis B
imageTetracycline for EGFR inhibitor-induced folliculitis B

Topical therapy

Systemic therapy

Second-line therapies

Oral antimicrobials
imageTigecycline and vancomycin for MRSA A
Other treatment modalities
imageIntramuscular immune globulin B
imagePhotodynamic therapy D
imageKetoconazole for Pityrosporum spp. D

image

[/level-membership-for-dermatology-category][not-level-membership-for-dermatology-category]

Folliculitis

Maricarr Pamela M. Lacuesta and Robert G. Phelps

Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports

image

Folliculitis is inflammation of the pilosebaceous follicle. Inflammation limited to the superficial portion of the follicle clinically presents with erythematous papules and pustules, while deeper involvement manifests with furuncles and abscesses. Etiologic factors include both infectious and non-infectious agents.

Bacterial pathogens are the predominant causes of infectious folliculitis. These include Gram-positive Staphylococcus aureus, Micrococcus, Streptococcus pyogenes and Clostridium perfringens, Gram-negative Pseudomonas, Klebsiella, Proteus, Enterobacter and Citrobacter spp., Acinetobacter baumannii and Aeromonas hydrophila, Treponema pallidum and mycobacteria. Herpes and molluscum cause viral folliculitis while Candida spp., Pityrosporum spp., Rhodotorula spp., Trichosporon cutaneum and dermatophytes cause fungal folliculitis. Parasitic folliculitis may be due to Demodex spp., scabies or larva migrans. Definitive diagnosis is achieved by identification of the infectious agent/s; however, thorough history taking and detailed physical examination may provide helpful clues to the diagnosis. For example, atopic patients are particularly susceptible to staphylococcal folliculitis; a lamellar circle of desquamation surrounding the papules or pustules is a valuable clinical finding.

There should be a high index of suspicion for Gram-negative folliculitis in acne patients treated with long term antibiotics. Exposure to contaminated water in pools or jacuzzis can lead to folliculitis by Pseudomonas aeruginosa or Aeromonas hydrophila. Candida folliculitis is a frequent finding in individuals with heroin addiction and one form may preferentially affect the male beard area. Pityrosporum folliculitis, favoring the upper trunk, is more commonly found in regions with hot and humid climate and has recently been reported in a Crohn disease patient treated with infliximab. Demodex folliculitis is suggested by rosacea-like lesions on the face with periorificial accentuation. This is common among young pubescent patients but may also be associated with HIV infection or leukemia. Immunocompromised patients, most notably with HIV infection, develop not only widespread folliculocentric lesions caused by bacteria, viruses or parasites but also a characteristic sterile eosinophilic pustular folliculitis which is paradoxically related to both immune suppression and reconstitution. The clinician should utilize laboratory examinations that aid in the isolation of the infectious agents.

Non-infectious folliculitis may be associated with mechanical factors (friction, occlusion or follicular trauma), of which epilation is an example. Folliculitis has also been reported to develop over the recipient area after hair transplantation. Coal tar and cutting oils cause irritant folliculitis while sun exposure causes actinic folliculitis. Other associations include rheumatologic disorders (Behçet disease, Reiter syndrome, systemic lupus erythematosus, mixed connective tissue disease, and rheumatoid arthritis), inflammatory bowel disease, blood dyscrasias, and pregnancy. Perforating folliculitis is not only associated with diabetes mellitus and renal failure but also with TNF-α inhibitors (infliximab). The etiopathogenic mechanism for necrotizing infundibular crystalline folliculitis (waxy papules with folliculocentric filamentous birefringent crystalline deposits) is hypothesized to be physical/chemical injury or yeast and bacterial action.

Agents responsible for drug-induced folliculitis include epidermal growth factor receptor (EGFR) inhibitors, TNF-α inhibitors, trastuzumab, sorafenib, lapatinib, lenalidomide, lithium, halogens, anti-tuberculous medications, and corticosteroids.