Folliculitis Causes and Treatments
Folliculitis is caused by infection or irritation of individual hair follicles. Patients with folliculitis present with pustules at the bases of hairs, particularly on the scalp, back, legs, and arms (Fig. 33-38). Folliculitis occurs more often in obese, immunocompromised, or diabetic patients. S. aureus is the most common pathogen. A form of folliculitis caused by Pseudomonas, hot tub folliculitis, occurs when patients use poorly maintained hot tubs. The condition may be self-limited, requiring only the use of antibacterial soap, or may persist and require topical or systemic antibiotic therapy. If a pseudomonal infection is suspected and lesions persist for more than 5 days without treatment, an oral fluoroquinolone (e.g., ciprofloxacin) should be considered.
Extensive serous weeping, folliculitis, and pyoderma indicate bacterial infection usually secondary to S. aureus in patients with AD. The concept that infection with S. aureus can exacerbate acute AD, and colonization promotes chronic skin inflammation, provides a rationale for use of anti-staphylococcal therapy in patients with poorly controlled AD. Systemic anti-staphylococcal antibiotics are particularly helpful in the treatment of acute exacerbations of AD due to diffuse S. aureus infection.55-57 Erythromycin and the newer macrolide antibiotics (azithromycin and clarithromycin) are usually beneficial for patients who are not infected with a macrolide-resistant S. aureus strain. However, for macrolide-resistant S. aureus, a penicillinase-resistant penicillin (e.g. dicloxacillin) should be used. First-generation cephalosporins also offer effective coverage for S. aureus. Topical mupirocin is useful in the treatment of localized impetiginized skin lesions.5
Many clinical studies demonstrate that the colonisation of the skin and subsequent sensitization to Malassezia yeasts can trigger skin inflammation and play a role in the pathogenesis of AD. Malassezia yeasts are members of the normal human cutaneous flora but on the other hand these fungi are associated with different skin diseases such as pityriasis versicolor, Malassezia folliculitis and sebor-rhoeic dermatitis.
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Coal tar is keratolytic and may have antiproliferative and anti-inflammatory ef-fects.2 Coal tar products include crude coal tar and tar distillates (liquor carbonis de-tergens) available as ointments, creams, and shampoos in various strengths. Preparations containing coal tar may precipitate folliculitis,10 will stain clothing, and have an unpleasant odor. They are also photosensitizing and can be combined with ultraviolet B (UVB) phototherapy (Goekermann's regimen) to increase treatment response.17
Erythema toxicum neonatorum is a benign, self-limited eruption of unknown etiology that occurs in up to 70 of term newborns characterized by discrete, small, erythematous macules or patches up to 2 to 3 cm in diameter with 1- to 3-mm firm pale yellow or white papules or pustules in the center. The trunk is predominantly involved. This rash usually presents within the first 24 to 72 hours of life. The distinctive feature of erythema toxicum is its evanescence or disappearance with each individual lesion usually disappearing within 2 or 3 days. New lesions may occur during the first 2 weeks of life. The neonate should appear well and lack any systemic signs of illness other than occasional peripheral eosinophilia. Wright-stained slide preparations of the scraping from the center of the lesion demonstrate numerous eosinophils. The differential diagnosis includes transient neonatal pustular melanosis, newborn milia, miliaria, neonatal herpes simplex, bacterial folliculitis, candidiasis,...
It can be classified into scarring (absence of follicles) and nonscarring (presence of follicles) alopecia. Scarring alopecia is commonly caused by discoid lupus erythematosus (erythematous mottled pigmentation and atrophic scalp scarring) and folliculitis decalvans (multiple crops of pustules on the scalp). Occasionally, prolonged bacterial and inflammatory fungal infections (kerion) can induce scarring on the scalp. Nonscarring alopecia results from alopecia areata (annular areas of alopecia on the scalp or beard area), telogen effluvium (diffuse scalp shedding of hair 2 to 3 months after a stressful event, illness, or new medication), anagen effluvium (diffuse scalp shedding after chemotherapy), trichotillomania (constant pulling of the hair), traction alopecia (chronic tension of braided hair causing alopecia), and tinea capitis. Syphilis can cause a patchy, moth-eaten alopecia.
History should be obtained including a review of risk factors for HIV-1 exposure, drug and alcohol history, sexual history, travel history, and medical history. A complete baseline physical examination should be performed. Focused follow- up examinations are then recommended with attention directed to findings that indicate disease progression such as general appearance and weight loss, dermatological conditions (seborrheic dermatitis, folliculitis, dermatophytosis, Kaposi's sarcoma, bacillary angiomatosis), oral lesions (candidiasis, hairy leukoplakia, aphthous ulcers, periodontal disease), localized lymphadenopathy, splenomegaly and signs or symptoms of neurological neuropsychiatric involvement (mood or affective disorders, psychomotor slowing, abnormal eye movements, hyperreflexia, change of gait).
The folliculitis usually involutes in 7 to 10 days without treatment, although ciprofloxacin may be used. Acetic acid compresses and local wound cleansing may speed recovery. In addition, the hot tub or source of exposure must be decontaminated to avoid reexposure. Hot Tub Folliculitis. Note the pustules localized to the hair follicles of the trunk and proximal extremity. (Photo contributor Jeffrey S. Gibson, MD.)
Dermatofibromas (benign fibrous histiocytomas) are most likely fibrous reactions to minor trauma, insect bites, viral infections, ruptured cysts, or folliculitis. The nodules can be found anywhere on the body, but most often appear on the legs and arms. Dermatofibromas are firm, raised papules, plaques, or nodules that vary from 3 to 10 mm in diameter (Fig. 33-76). Dermatofibromas have a central fibrous scar and often have a hyperpigmented or pink halo around the central hypopigmented area. This has a characteristic pattern on dermoscopy.
Eosinophilic folliculitis, commonly seen in advanced HIV patients, is a pruritic skin eruption usually involving the face, neck, trunk, and extremities manifesting in the form of pustules and papules. The skin lesions usually start as small pustular groups that later coalesce to create irregular erosions and plaques with central hyperpigmentation. The associated pruritus is often so intense that the lesions become excoriated. Most patients with this condition will demonstrate CD4 cell counts of less than 250 u L. Approximately half of these patients will have moderate eosinophilia and moderate leukocytosis. The etiology of eosinophilic folliculitis is unknown, but is commonly thought of as an inflammatory process associated with immune dysfunction. It has become less common with the advent of highly active antiretroviral therapy.