Folliculitis, Acute Bacterial [Bockhart's Impetigo, Superficial Pyoderma, "Hot Tub" Folliculitis, Sycosis Vulgaris [Barbae] or Barbers Itch, Furuncles [Boils], Carbuncles)

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).

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).

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.

Figure 3.

“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.

• Diagnosis confirmation

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?

• Etiology

Folliculitis is a primary inflammation of the hair follicle that occurs as a result of various infections, or secondary to follicular trauma or occlusion.

• Pathophysiology

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.

Figure 4.

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.

Treatment Options

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.

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