Natural Treatment to get rid of Folliculitis
Final common pathway of various types of chronic folliculitis, producing progressive scarring Dissecting folliculitis lupus erythematosus lichen planopilaris kerion pseudopelade of Brocq follicular degeneration syndrome pemphigus vulgaris pemphigus foliaceus Darier disease Hailey-Hailey disease pseudofolliculitis barbae Brooke RC, Griffiths CE (2001) Folliculitis decalvans. Clinical & Experimental Dermatology 26(l) i20-122
Ofuji's disease Ofuji disease eosinophilic folliculitis HIV-associated eosinophilic fol liculitis HIV-related eosinophilic folliculitis, sterile eosinophilic pustulosis eosinophilic pustular dermatosis infantile childhood eosinophilic pustulosis of the scalp Other forms of folliculitis, including bacterial and fungal varieties pustular psoriasis acne rosacea perioral dermatitis scabies candidiasis folliculitis decalvans insect bite reaction Langerhans cell histiocytosis follicular mucinosis superficial pemphigus Lazarov A, Wolach B, Cordoba M, Abraham D, Vardy D (1996) Eosinophilic pustular folliculitis (Ofuji disease) in a child. Cutis 58(2)1135-138
Folliculitis, eosinophilic pustular 247 Hot tub folliculitis caused by psedo-monas organisms in tub or pool water pruritic, edematous, erythematous papules or pustules in areas of skin occluded by a bathing suit Pityrosporum folliculitis pruritic acne-form papules on the upper back, chest, upper arms, neck, chin, and sides of the face caused by yeast forms of Pityrospo-rum ovale Fungal folliculitis caused by candidal species and dermatophytes principle etio-logic agents Trichophyton verrucosum and Trichophyton mentagrophytes affects the coarse hairs in the mustache and beard area in men taphylococcal folliculitis follicular-based red papules and pustules, caused by Staphylococcal aureus
Lymphomatoid granulomatosis affects usually adults, but cases have been described in children (2). The most common sites of involvement are the lungs. Almost all patients have pulmonary manifestations during their disease course. The other two commonly involved organs are the brain and kidneys. Malignant lymphoma involving lymph nodes develop in 12 of patients. About 50 of the patients with LYG have skin involvement (3). Exclusive cutaneous involvement is rare and may be associated with a better outcome. The clinical features of cutaneous LYG are extremely diverse (4) and generally transient (5). Multiple erythematous dermal papules and or subcutaneous nodules, with or without ulceration, facial edema, and folliculitis-like eruptions (5-7) may be present. Frequently, patients who have
Gram-negative folliculitis is characterized by the sudden development of superficial pustules in patients suffering from long-standing acne, rosacea or folliculitis treated with oral or topical antibiotics. The long-term use of antibiotics creates an ecological imbalance of micro-bial flora, with suppression of the gram-positive resident organisms. A variety of gram-negative bacteria are involved, including Pseudomonas and Enterobacteriaceae. Folliculitis caused by colonization with S. aureus or S. epidermidis on the face can be sometimes misdiagnosed as acne. The prominent lesions are superficial follicular pustules that are often distributed on the lateral cheeks, the chin and the temporal sites of the forehead. The rare folliculitis due to Candida may also present as multiple pustular eruptions.
Application of topical corticosteroids (CSs) is part of the standard external therapy in CLE. Alone or in combination with systemic anti-inflammatory agents, CSs are very effective in reducing the main symptoms of the skin lesions of LE, namely, redness and squamae. To be effective in LE, intermediate (e. g., triamcinolone acetonide) to potent or superpotent CS preparations (betamethasone dipropionate, halobetasol propionate, fluocinonide, and clobetasol propionate) have to be used to achieve significant amelioration of the skin lesions. Usually, potent CS preparations should not be used on the face since the well-known side effects (atrophy, telangiectasias, steroid dermatitis, and folliculitis) tend to be especially severe in facial skin. However, in view of the risk-benefit ratio, CLE represents an exception to that rule, since the facial skin lesions of LE are often exceedingly disfiguring so that the CS side effects are less troublesome. Twice-daily application for a few weeks...
Folliculitis decalvans, which in its active stages can hardly be confused with DLE because of its pustules and crusts, eventually leads to cicatricial alopecia, which is morphologically similar to that of lichen planopilaris (small areas of alopecia intermingled with tufts of normal hair, most often in the parietal and occipital areas). Similar hairless scars, although less extensive, may arise from furuncles and trichophytic infections (Kerion Celsi type).
Chronic staphylococcal folliculitis and TB may be very difficult to distinguish because TB usually has a component of secondary infection that will respond to broad-spectrum antibiotics. One should always be suspicious when there is rapid relapse of a facial folliculitis after appropriate antimicrobial therapy. Gram-negative folliculitis can also be confused with TB however, the pustules are usually painful and not pruritic. They are dusky red and have a straw-colored surface pustule. Bacterial culture will usually distinguish between them.
Furuncles are hair follicles infected with S. aureus and present as yellow-headed pustules. They are commonly seen on the back of the neck in men or in patients treated with ointments or tar (particularly if the skin has been occluded). Extensive areas of folliculitis (furuncles) will require systemic floxacillin (flucoxacillin), but solitary or isolated lesions will respond to topical mupirocin or sodium fusidate (Fucidin). Mupirocin (pseudomonic acid) interferes with bacterial protein synthesis, has the advantage of no cross-resistance with other antibiotics and is available only as a topical preparation. It is effective against both staphylococci and streptococci and may be used in the treatment of folliculitis, infected eczema, and as prophylaxis against nasal carriage of staphylococci. Fucidic acid inhibits bacterial protein synthesis and is particularly effective against staphylococcal skin infections. Topical
Series, folliculitis due to Pseudomonas aeruginosa O-11 from a hospital water supply rapidly developed into ecthyma gangrenosum in six hospitalized immunosuppressed patients (2). This represents a common scenario in which early lesions resemble a bacterial folliculitis, and then rapidly progress to typical ecthyma gangrenosum lesions. In the largest series of patients with ecthyma gangrenosum, over 75 were felt to originate in the skin, and two thirds primarily involved apocrine areas. Some patients developed septicemia (1).
HISTOPATHOLOGY The lesions of rosacea are variable. There may be only telangiectatic vessels with a mild to moderate perivascular infiltrate of lymphocytes containing a small number of plasma cells. Papulopustular rosacea lesions have more intense inflammation that is both perivascular and around hair follicles. Active pustular lesions have a superficial folliculitis, while older lesions may have loosely associated granulomas adjacent to follicles. Granulomatous rosacea has tuberculoid granulomas with epithelioid cells, multinucleated giant cells of Langhans and foreign-body types, and a substantial rim of lymphocytes and plasma cells. The granulomas may be centered on ruptured hair follicles. The granulomas may have central necrosis ( caseat-ing necrosis ) in approximately 10 of cases.