1887

Abstract

and are normal skin inhabitants that are frequently isolated from lesions caused by acne, and these micro-organisms are considered to contribute to the inflammation of acne. In the present study, we examined the antimicrobial susceptibilities and resistance mechanisms of and isolated from patients with acne vulgaris in a university hospital in Japan from 2009 to 2010. Additionally, we analysed the relationship between the antimicrobial resistance of and the severity of acne vulgaris. Some strains (18.8 %; 13/69) were resistant to clindamycin. All strains had a mutation in the 23S rRNA gene, except for one strain that expressed (X) encoding a 23S rRNA methylase. Tetracycline-resistant strains were found to represent 4.3 % (3/69) of the strains, and this resistance was caused by a mutation in the 16S rRNA gene. Furthermore, three strains with reduced susceptibility to nadifloxacin (MIC = 16 µg ml) were detected. When analysing the correlation between the antimicrobial resistance of and , more than 80 % of the patients who carried clindamycin-resistant also carried clindamycin-resistant . However, no epidemic strain that exhibited antimicrobial resistance was detected in the strains when analysed by PFGE. Therefore, our results suggest that the antimicrobial resistance of is closely related to antimicrobial therapy. Additionally, those strains tended to be frequently found in severe acne patients rather than in mild acne patients. Consequently, the data support a relationship between using antimicrobial agents and the emergence of antimicrobial resistance.

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2014-05-01
2021-10-23
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