Trichophyton mentagrophytes kerion in a woman.
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Tufted folliculitis is an uncommon folliculitis of the scalp that resolves with patches of scarring alopecia within which multiple hair tufts emerge from dilated follicular orifices. The clinicohistological data from a group of 15 patients with tufted folliculitis were reviewed and compared with those of seven patients with folliculitis decalvans, five with acne keloidalis nuchae, four with dissecting cellulitis of the scalp, three with kerion celsi and 20 with follicular lichen planus. It was found that tufted folliculitis could be differentiated from folliculitis decalvans only by finding several hair tufts scattered within patches of scarring alopecia. Histologically, a single tuft consisted of peculiar clustering of adjacent follicular units opening at the bottom of an epidermal depression. Conversely, the presence of keloidal plaques in acne keloidalis nuchae, coalescing nodules discharging purulent material in dissecting cellulitis of the scalp, erythematous plaques covered by pustules replete with fungal elements in kerion celsi, and the absence of follicular pustules in follicular lichen planus distinguished these diseases from tufted folliculitis. On the basis of these findings, it is suggested that tufted folliculitis should be considered as a distinctive clinicohistological variant of folliculitis decalvans. Tufting of hair is caused by clustering of adjacent follicular units due to a fibrosing process and to retention of telogen hairs within the involved follicular units.
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In a series of 18 patients with folliculitis decalvans attending the Oxford hair clinic, eight were found to have areas of tufted folliculitis either at presentation or follow-up. There was no difference between these two groups in their presentation, clinical course, growth of causative organism (Staphylococcus aureus) or investigations including histology. We suggest that these two entities form part of a spectrum of a single disease. We performed lymphocyte staining on affected scalp biopsies, including CD4: CD8 and T-cell/B-cell ratios, but found no evidence of local immune suppression or failure which would explain the abnormal host response to a common pathogen in this rare condition. We introduced a new treatment regimen for these patients, oral rifampicin and oral clindamycin together for 10 weeks. Ten of the 18 patients have responded well with no evidence of recurrence 2-22 months after one course of treatment, and 15 of the 18 responded after two or three courses.
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Two children are described with the combination of aplasia cutis congenita (ACC) and transverse limb defects known as Adams-Oliver syndrome. Whereas in the first child the typical features of ACC, syndactyly and transverse nail dystrophy were only mildly expressed and associated defects of the central nervous system and cardiac malformations were absent, the second child suffered from a very severe expression of the syndrome, with a combination of ACC, syndactyly, cutis marmorata telangiectatica congenita and multiple cardiac and central nervous system malformations which resulted in fatal central respiratory insufficiency.
A rising prevalence of head lice among school children and rising sales of insecticides with anecdotal evidence of their treatment failure, led us to examine whether head lice in Bristol and Bath were resistant to the insecticides available for treating head lice. Ten schools in Bristol and Bath were visited to collect field samples of head lice. A comparison was made of the survival rates of fully sensitive laboratory reared body lice and field samples of head lice on insecticide exposure. To confirm the in vitro relevance of these tests we performed supervised treatments of affected subjects with malathion or permethrin. There were significant differences (P < 10-6 Fishers exact test) between head and body lice survival for malathion and permethrin exposure, but not for carbaryl. There was an 87% failure rate for permethrin and a 64% failure rate for malathion with the topical treatment of a selected number of infested school children. We conclude that there is a high resistance to permethrin and malathion, but head lice remain fully sensitive to carbaryl. This is the first report of doubly resistant head lice. As permethrin, phenothrin (a very similar synthetic pyrethroid) or malathion are the active ingredients in all the over-the-counter head lice treatments in the U.K., then it is likely that head lice prevalence will continue to increase. The resistance against permethrin employed by the head louse is probably the kdr (knockdown resistance) mechanism, and an enzyme-mediated malathion-specific esterase is the likely mechanism against malathion.
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BACKGROUND: Actinic keratoses (AK) are premalignant lesions, which are routinely treated by destructive procedures such as cryotherapy, electrodessication or topical 5-fluorouracil. OBJECTIVES: The aim of this study is to report six cases of AK treated with a potential new topical therapy, imiquimod. METHODS: Subjects included in this study had suffered with recurrent AK for between 5 and 16 years. All six men were treated with imiquimod 5% cream three times a week for 6-8 weeks. In the event of a local skin reaction treatment was modified to two times per week. RESULTS: All the AK lesions were successfully cleared after treatment with imiquimod cream 5% for 6-8 weeks. Histologically, no apparent signs of persisting AK could be detected, and no recurrences were reported during follow up. CONCLUSIONS: This study suggests that imiquimod may be useful as a new therapy for the treatment of actinic keratoses.
Scalp actinic keratoses (AKs) are common, particularly in elderly bald males. Cryotherapy and 5-fluorouracil are effective for localized AKs but are limited in extensive disease. Topical 5-aminolaevulinic acid photodynamic therapy (5-ALA PDT) is an alternative. We treated four patients with extensive scalp AKs with low light dose, low dose-rate topical 5-ALA PDT using a broad-spectrum visible light source. Three patients cleared and one showed significant improvement. Remission lasted 6 months.
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