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Recovery of susceptibility to penicillin G in clinical isolates of Streptococcus pneumoniae despite increased accumulation of pbp gene alterations

https://asahikawa-med.repo.nii.ac.jp/records/1337
https://asahikawa-med.repo.nii.ac.jp/records/1337
b5eefe53-e8c2-4fe2-b4e3-288e73084061
名前 / ファイル ライセンス アクション
1622.pdf 1622.pdf (537.3 kB)
Item type 学術雑誌論文 / Journal Article_02(1)
公開日 2009-03-11
タイトル
タイトル Recovery of susceptibility to penicillin G in clinical isolates of Streptococcus pneumoniae despite increased accumulation of pbp gene alterations
言語 en
言語
言語 eng
資源タイプ
資源タイプ journal article
著者 大崎, 能伸

× 大崎, 能伸

大崎, 能伸

ja-Kana オオサキ, ヨシノブ

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Tachibana, M

× Tachibana, M

Tachibana, M

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Awaya, T

× Awaya, T

Awaya, T

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Kuroki, M

× Kuroki, M

Kuroki, M

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Ito, Y

× Ito, Y

Ito, Y

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著者 ローマ字
Ohsaki, Yoshinobu
書誌情報 International Journal of Antimicrobial Agents

巻 32, 号 5, p. 427-431, 発行日 2008-11-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 0924-8579
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.1016/j.ijantimicag.2008.05.002
リンクURL
内容記述タイプ Other
内容記述 http://dx.doi.org/10.1016/j.ijantimicag.2008.05.002 | http://dx.doi.org/10.1016/j.ijantimicag.2008.05.002
抄録
内容記述タイプ Abstract
内容記述 Two hundred consecutive clinical isolates of S. pneumoniae in 2005 and 2006 wereanalyzed for susceptibility to antimicrobials, pbp alterations and macrolide resistant gene expressions (2007 analysis). The results were compared with our previous data (2003 analysis). The average minimum inhibitory concentration (MIC) of penicillin G (PEN-G) in isolates with 1a^m/2x^m/2b^m decreased from 1.135±0.503 mg/L in the 2003 analysis to 0.872±0.540 mg/L in the 2007 analysis (p=0.0046). Isolates with 1a^m/2x^m/2b^m increased from 30.5% to 32.3% but the difference was not statistically significant (p=0.6979). Isolates with a MIC of clarithromycin ≥1.0 mg/L increased from 65.9% to 80.0% (p=0.0005). Isolates with ermB expression increased from 46.6% to 62.6% (p=0.0004). We concluded that the decrease of penicillin resistance of S. pneumoniae did not correlate with a decrease in pbp mutations; on the contrary, isolates with pbp mutations increased. A decrease of penicillin resistance in S. pneumoniae with the pbp mutation seemed to explain our present results about the recovery of penicillin susceptibility. Our results suggested that the spread of mutated pbp genes among S. pneumoniae itself is not responsible for the acquisition of the penicillin-resistant phenotype. Use of β-lactams, especially oral cephalosporins, seems to be responsible for the acquisition of penicillin resistance.
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出版タイプ AM
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