A pediatric case of generalized lichen aureus.

Lichen aureus is a particularly rare subtype of pigmented purpuric dermatosis and is characterized by the sudden appearance of golden or rust-colored macules or needle-tip-sized flat papules (concentrated in one region to form lichenoid papules) on the lower limbs. These skin lesions are usually confined to an isolated, unilateral distribution, and linear segmental distribution is rare. In this report, we have documented one such case, where the lesions on the limb were arranged in strips (segmental distribution) that roughly followed the direction of the venous drainage. And the first attack and subsequent aggravation were both associated with the onset of allergic rhinitis, a Type I hypersensitivity.

Differences in 23S ribosomal RNA mutations between wild-type and mutant macrolide-resistant Chlamydia trachomatis isolates.

The aim of the present study was to determine the in vitro susceptibility of wild-type and mutant clinical isolates of Chlamydia (C.) trachomatis strains to erythromycin, azithromycin and josamycin, and to identify the resistance-conferring 23S ribosomal (r)RNA mutations in the isolates. The wild-type resistant isolates were defined as those with minimum inhibitory concentration values above the tissue concentration of the antibiotic in the urogenital system. Furthermore, all resistant C. trachomatis isolates were exposed to sub-inhibitory concentrations of macrolides, and 13 resistant mutants were selected following serial passages. Among the 8 wild-type isolates that were resistant to erythromycin, 3 isolates had a mutation at T2611C in the 23S rRNA gene while the others did not show any 23S rRNA mutations. The selected mutant isolates showed a 4- to 16-fold reduction in in vitro sensitivities. With regard to the mutant strains, the T2611C mutation was found in 10 isolates, A2057G mutation in 6 isolates, and A2059G mutation in 1 isolate. Thus, the macrolide-resistant isolates of the wild-type strain had different mutations from those selected by exposure to sub-inhibitory concentrations of macrolides. Also, since 23S rRNA mutations were not identified in certain isolates, it was considered that other molecular mechanisms may also be responsible for the macrolide resistance of C. trachomatis.