Are You Confident of the Diagnosis?
Characteristic findings on physical examination
Acute bacterial folliculitis (ABF)takes various forms:
The most common superficial form of infectious folliculitis is known as impetigo of Bockhart and is caused by Staphylococcus aureus. Clinically it is characterized by 1-6mm erythematous follicular-based papules or fragile pustules that may rupture and leave a yellow crust. The pustule is often pierced by a hair that is easily extracted from the follicle (Figure 1).
Lesions are most commonly located on the head and neck, trunk, extremities, buttocks, and axillae. The lesions can be tender, painful, or simply pruritic. Because of the superficial nature of the process, scarring is uncommon. Up to 20% of patients with bacterial folliculitis experience recurrent disease, which may be the result of community-type methicillin-resistant Staphylococcus aureus.
Furuncles are a deep form of folliculitis that typically involves the entire hair follicle and the surrounding subcutaneous tissue. Coalescence of several furuncles results in a carbuncle or subcutaneous abscess. Patients present with a tender, erythematous nodule, often with a central pustule that may drain on its own (Figure 2).
Sycosis vulgaris, also known as sycosis barbae or barber’s itch, is a type of deep folliculitis seen mostly in post-puberty males, usually in the third and fourth decades of life. The lesions begin with an inflammatory follicular papule or pustule located in the beard and accompanied by a burning sensation, which is aggravated by shaving. Gradually, more pustules develop and eventually coalesce into scaly patches or plaques studded with pustules (Figure 3). The chronic form may go on for years and in severe cases, the follicles are completely destroyed by scarring.
“Hot tub” folliculitis is a condition that arises when water sanitation is less than optimal and a transient infection by Pseudomonas aeruginosa occurs. Pseudomonas can survive in the hot water of whirlpools, swimming pools, and physiotherapy pools if the pH and chlorine content are not controlled properly.
Expected results of diagnostic studies
Usually the diagnosis of bacterial folliculitis is made based upon the results of clinical history and physical examination; however, in cases resistant to standard therapy, cultures, Gram stain, potassium chloride (KOH) preparation, and biopsy are the diagnostic tests of choice.
The differential diagnosis includes other forms of folliculitis that arise from fungal infections (Pityrosporum folliculitis, tinea barbae, and Majocchi’s granuloma), herpes, Demodex, or gram-negative bacteria. In addition, drug-induced folliculitis, acute generalized pustulosis, pseudofolliculitis barbae, eosinophilic folliculitis, acne, keratosis pilaris, impetigo, miliaria, and an id reaction should be considered in the differential.
These entities can be sorted out by bacterial, viral, or fungal cultures (or polymerase chain reaction [PCR]); combined with skin biopsies, Gram stains for bacteria, periodic acid-Schiff (PAS) stains for fungi, or a Tzanck preparation (with or without direct immunofluorescence) for herpes.
Who is at Risk for Developing this Disease?
Although the exact incidence is unknown, folliculitis is a relatively common condition, occurring in all races with no gender predilection. There are several risk factors that increase a person’s susceptibility to folliculitis. These include frequent shaving or chronic friction from clothing, immunosuppression, preexisting dermatoses, long-term antibiotic or steroid use, occlusive clothing and/or occlusive dressings, exposure to hot temperatures and high humidity, chronic nasal carriage of Staphylococcus aureus, exposure to certain oils and chemicals, diabetes mellitus, obesity, and use of epidermal growth factor receptor (EGF-R) inhibitor medications.
What is the Cause of the Disease?
Folliculitis is a primary inflammation of the hair follicle that occurs as a result of various infections, or secondary to follicular trauma or occlusion.
Bacterial folliculitis is characterized histologically by the presence of inflammatory cells within the wall and ostia of the hair follicle, associated with bacterial colonization, most commonly by Staphylococcus aureus. The inflammation can be limited to the superficial aspect of the follicle, primarily involving the infundibulum (Figure 4), or the inflammation can affect both the superficial and deep aspect of the follicle.
Systemic Implications and Complications
Systemic symptoms are infrequent, but fatigue, fever, or chills can occasionally be seen in patients who develop carbuncles. Most cases of superficial folliculitis resolve without complications; however, scarring can be seen in more substantial infections.
For recurrent uncomplicated superficial folliculitis, use of antibacterial soaps and good hand washing may be all that is needed. For refractory or deep lesions secondary to gram-positive organisms, empiric treatment with topical and/or oral antibiotics may be beneficial.
Since S aureus is the most common pathogen, systemic therapy must cover this organism, as well as other gram-positive bacteria. S. aureus is penicillin resistant; therefore, dicloxacillin or a cephalosporin is the first line of treatment. Methicillin-resistant organisms are becoming more common, and treatment may require clindamycin, trimethoprim-sulfamethoxazole, minocycline, or linezolid. The newest medications that have been approved for methicillin-resistant S. aureus (MRSA) infections are ceftaroline, dalbavancin, oritavancin, and tedizolid.
If a pateint does not improve with a standard course of antibiotics, other causes of folliculitis must be investigated.
For recurrent and recalcitrant folliculitis, mupirocin ointment in the nasal vestibule twice a day for 5 days may eliminate the S. aureus carrier state. Family members also may be nasal carriers of S. aureus; the use of mupirocin ointment in the nasal vestibule twice a day for 5 days and/or 600mg/day of rifampin orally for 10 days is recommended.
For hot tub folliculitis, treatment is usually not needed, since the disease is self-limited; however, anti-pruritic medications may be used if needed. In recalcitrant cases or if the patient is immunocompromised, oral antipseudomonal antibiotics may be required.
For carbuncles and furuncles, warm compresses can promote maturation and drainage, but for fluctuant lesions, incision and drainage may be needed.
Optimal Therapeutic Approach for this Disease
Optimal treatments are summarized in Table I.
|First-line therapy||Antibacterial soap and good hygiene|
|Second-line therapy Topical and/or oral antibiotics to cover gram-positive organisms||Dicloxacillin 250mg every 6 hours for 7-10 days Cephalexin 250-500mg every 6 hours for 7-10 days|
|Third-line therapy Methicillin-resistant organisms||Trimethoprim-sulfamethoxazole DS: 160mg/800mg, twice a day for 10-14 days Minocycline 100mg, twice a day for 10-14 days Doxycycline 100mg, twice a day for 10-14 days Clindamycin 300mg, orally every 8 hours for 10-14 days*Linezolid 600mg, twice a day for 10-14 days|
|Fourth-line therapy Chronic recurrent lesions S. aureus carrier state||Mupirocin to nasal vestibule twice a day for 5 days and/or rifampin 600mg once a day for 10 days|
*D-zone test should be performed to identify inducible clindamycin resistance.
While lesions are active, avoid shaving irritated skin 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 and fungi.
Good personal hygiene, including bathing, hand washing, and keeping nails short and clean, reduces the risk of folliculitis. To eliminate clothing contamination, the patient’s clothing and bed and bath linens should be washed in hot water and not shared with family members. Wearing loose rather than snug-fitting clothing helps reduce friction. Most importantly, patient education to reduce predisposing factors helps decrease the risk of recurrence.
In the case of hot tub folliculitis, prevention should be directed at preventing the condition by appropriately cleaning the whirlpool or hot tub and maintaining appropriate chlorine levels in the water.
Unusual Clinical Scenarios to Consider in Patient Management
Over the last decade, targeted chemotherapeutic agents have been developed that inhibit epidermal growth factor receptor, and although these agents can be beneficial in the treatment of various neoplasms, they also result in a papulopustular drug eruption that resembles bacterial folliculitis. The eruption is follicular-based and primarily occurs on the face, chest, and upper back, approximately 2 weeks after initiation of chemotherapy.
This eruption is seen in up to 90% of patients taking EGF-R inhibitors. Since its presence correlates with positive response to chemotherapy, the eruption may be used as a clinical marker of response to treatment. These lesions are inflammatory and not infectious. Although they are responsive to the tetracyclines, the eruptions are due to the anti-inflammatory effect of the antibiotics.
The eruptions are graded by severity:
Grade 1: macular-papular eruption or erythema without associated symptoms
Grade 2: macular-papular eruption, erythema, or local desquamation covering less than 50% of body surface, associated with pruritus or other systemic symptoms
Grade 3: symptomatic generalized erythroderma or papulopustular eruption or desquamation covering greater than or equal to 50% of body surface area
Grade 4: generalized exfoliative or ulcerative dermatitis or bullous dermatitis
Grade 5: death
Optimal therapy remains controversial. For grade 1 lesions, usually no intervention is required, but for moderate eruptions, topical antibiotics or topical corticosteroids can be used, and in recalcitrant cases, oral antibiotics can be administered. For severe eruptions, the dose of the medication should be reduced or discontinued.
What is the Evidence?
Kelly, P, Bolognia, JL, Jorizzo, JL, Rapini, RP. “Folliculitis and the follicular occlusion tetrad”. Dermatology. vol. Vol 1. 2003. pp. 553-66. (Good overall dermatology textbook used by most residency training programs.)
High, WA, Schwarzenberger, K, Werchiak, AE, Ko, CJ. “Cutaneous infections”. Requisites in dermatology: general dermatology. 2009. pp. 100-1. (Good abbreviated textbook that goes over the most common dermatologic conditions.)
Blume, JE, Levine, EG, Heyman, WR, Bolognia, JL, Jorizzo, JL, Rapini, RP. “Bacterial disease”. Dermatology Vol 1. 2003. pp. 1125-6. (Good overall dermatology textbook used by most residency training programs.)
Zichichi, L, Asta, G, Noto, G. “Pseudomonas aeruginosa folliculitis after shower/bath exposure”. Int J Dermatol. vol. Apr;39. 2000. pp. 270-3. (This article reviews fourteen cases of Pseudomonas folliculitis and reviews etiology and clinical presentation.)
Satter, E. “Folliculitis”. (Review article on folliculitis.)
Luelmo-Aguilar, J, Santandreu, MS. “Folliculitis: recognition and management”. Am J Clin Dermatol. vol. 5. 2004. pp. 301-10. (Review article on folliculitis.)
Rathore, MH. “Optimal Bleach Concentration Required to Kill MRSA in Bath Water”. AAP Grand Rounds. vol. 21. 2009. pp. 3(Discusses how to do bleach baths)
Rodvold, KA, McConeghy, KW. “Methicillin-resistant Staphylococcus aureus therapy: past, present, and future”. Clin Infect Dis. vol. 58. 2014. pp. S20-7.
“Centers for Disease Control and Prevention. Treatment of MRSA Infections”. (Review of MRSA therapies)
Roé, E, García Muret, MP, Marcuello, E, Capdevila, J, Pallarés, 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 Sep. vol. 55. 2006. pp. 429-37.
Bragg, J, Pomeranz, MK. “Papulopustular drug eruption due to epidermal growth factor receptor inhibitors, erlotinib and cetuximab”. Dermatol Online J. vol. 13. 2007. pp. 1(Discusses the cutaneous side effects of the epidermal growth factor inhibitors.)
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- Are You Confident of the Diagnosis?
- Who is at Risk for Developing this Disease?
- What is the Cause of the Disease?
- Systemic Implications and Complications
- Treatment Options
- Optimal Therapeutic Approach for this Disease
- Patient Management
- Unusual Clinical Scenarios to Consider in Patient Management
- What is the Evidence?