Notes: Background Propionibacterium acnes is the target of antimicrobial treatments for acne vulgaris. Acquired resistance to erythromycin, clindamycin and tetracyclines has been reported in strains from diverse geographical loci, but the molecular basis of resistance, via mutations in genes encoding 23S and 16S rRNA, respectively, has so far only been elucidated for isolates from the U.K. Objectives To determine whether similar or different resistance mechanisms occur in resistant P. acnes isolates from outside the U.K. Methods The phenotypes and genotypes of 73 antibiotic-resistant strains of P. acnes obtained from the skin of acne patients in the U.K., U.S.A., France, Germany, Australia and Japan were compared. Antibiotic susceptibilities were determined by minimum inhibitory concentration (MIC) measurements, and polymerase chain reaction and DNA sequencing were used to identify mutations in genes encoding rRNA. Results Most erythromycin-resistant isolates (MIC90≥ 512 μg mL−1) were cross-resistant to clindamycin but at a much lower level (MIC90≥ 64 μg mL−1). As in the U.K., resistance to erythromycin was associated with point mutations in 23S rRNA in 49 of 58 strains. An A→G transition at Escherichia coli equivalent base 2058 was present in 24 strains. This gave a unique cross-resistance phenotype against a panel of macrolide, lincosamide and type B streptogramin antibiotics. Two further point mutations (at E. coli equivalent bases 2057 and 2059) were identified (in three and 22 isolates, respectively) and these were also associated with specific cross-resistance patterns originally identified in isolates from the U.K. However, nine of 10 erythromycin resistant-strains from Germany did not exhibit any of the three base mutations identified and, in six cases, cross-resistance patterns were atypical. Consistent with previous U.K. data, 34 of 38 tetracycline-resistant strains carried a base mutation at E. coli 16S rRNA equivalent base 1058. Tetracycline-resistant isolates displayed varying degrees of cross-resistance to doxycycline and minocycline, but isolates from the U.S.A. had higher MICs for minocycline (4–16 μg mL−1) than isolates from other countries and, in particular, Australia. All the P. acnes isolates resistant to one or more of the commonly used antiacne antibiotics were sensitive to penicillin, fusidic acid, chloramphenicol and the fluoroquinolone, nadifloxacin. All but one isolate (from the U.K.) were sensitive to trimethoprim. Conclusions This study shows that 23S and 16S mutations identified in the U.K. conferring antibiotic resistance in P. acnes are distributed widely. However, resistant strains were isolated in which mutations could not be identified, suggesting that as yet uncharacterized resistance mechanisms have evolved. This is the first report of high-level resistance to minocycline and is of concern as these strains are predicted to be clinically resistant and are unlikely to remain confined to the U.S.A. Epidemiological studies are urgently required to monitor how resistant strains are selected, how they spread and to ascertain whether the prevalence of resistance correlates with antibiotic usage patterns in the different countries.

Notes: We report a case of bleomycin-induced flagellate dermatitis. Our patient developed pruritic linear lesions 4 days after her first dose of bleomycin. A closed patch test was performed, and was negative. However, on rechallenge, the linear eruption recurred in the previously involved sites, and in new sites, within 24 h. Flagellate dermatitis is a characteristic reaction to bleomycin use, but varying histological features and clinical presentations may be seen.

Notes: Dapsone at doses of 0·5 to 5·0 μ/ml was found to produce a dose-dependent inhibition of opsonized zymosan-induced human polymorphonuclear leukocyte(PMN) chemiluminescence (CL) in vitro. Simultaneous exposure of PMN to dapsone and zymosan was as effective in reducing CL as preincubation of PMN with dapsone. Preincubation of PMN with dapsone followed by washing, resulted in the loss of dapsone-mediated CL inhibition, indicating that dapsone did not permanently alter the CL-generating mechanism and that the drug had to be present to inhibit CL. Dapsone did not absorb light at the wavelength of CL and was not toxic to PMN at concentrations tested. Sodium azide, an inhibitor of myeloperoxidase-mediated CL inhibited PMN CL to the same degree as dapsone. When incubated together with PMN, dapsone and azide did not produce an additive inhibition of CL. These data suggest that inhibition of myeloperoxidase may be the mechanism by which dapsone inhibits PMN CL.

Notes: Background  Skin colonization by antibiotic-resistant propionibacteria is commonplace among acne patients globally. Increasing attention is now being paid to how resistance rates might be reduced to preserve the future efficacy of antibiotics, especially erythromycin and clindamycin in acne therapy.Objective  To assess the efficacy of oral isotretinoin in the control of antibiotic-resistant propionibacteria.Methods  Acne patients (72 in the U.K., 62 in the U.S.A.) colonized with high numbers of antibiotic-resistant propionibacteria were sampled before, during and 12 weeks after oral isotretinoin therapy. Propionibacterial samples were collected from five acne-prone skin surface sites using a detergent scrub method and from the anterior nares using moistened swabs. Total and antibiotic-resistant propionibacteria were enumerated by viable counting on media with and without selective antibiotics.Results  After 16 weeks of oral isotretinoin therapy, mean population densities of viable propionibacteria and variants resistant to erythromycin, clindamycin or tetracycline had fallen by more than 90% at all skin sites and in the nares. The sole exception was a smaller reduction in tetracycline-resistant strains on the lower back. In general, greater reductions were observed on skin than in the nares. By the end of the treatment period only three patients (all in Philadelphia) yielded no antibiotic-resistant strains from any site. Post-treatment, propionibacterial counts remained well below pretreatment levels but had begun to recover on the face and in the nares. The recovering propionibacterial population included both susceptible and resistant strains. Changes during and post-treatment at the two centres were similar but not identical.Conclusions  Oral isotretinoin effectively reduced skin and nasal colonization by antibiotic-resistant propionibacteria. However, viable populations of resistant isolates persisted post-treatment at multiple sites. Novel methods are required to eradicate antibiotic-resistant propionibacteria completely, especially from the nasal reservoir.

Notes: Tetracycline, declomycin and erythromycin, in concentrations lower than the minimal inhibitory dosages, were shown to inhibit lipase production by Propionibacterium acnes in vitro.