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- Yuji Morita
- Department of Microbiology, School of Pharmacy, Aichi Gakuin University/ 1-100 Kusumoto, Chikusa, Nagoya, Aichi 464-8650, Japan
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- Junko Tomida
- Department of Microbiology, School of Pharmacy, Aichi Gakuin University/ 1-100 Kusumoto, Chikusa, Nagoya, Aichi 464-8650, Japan
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- Yoshiaki Kawamura
- Department of Microbiology, School of Pharmacy, Aichi Gakuin University/ 1-100 Kusumoto, Chikusa, Nagoya, Aichi 464-8650, Japan
書誌事項
- 公開日
- 2012-11-21
- 資源種別
- journal article
- 権利情報
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- https://creativecommons.org/licenses/by/3.0/
- DOI
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- 10.3390/antibiotics1010029
- 公開者
- MDPI AG
説明
<jats:p>Helicobacter cinaedi causes infections, such as bacteremia, diarrhea and cellulitis in mainly immunocompromised patients. This pathogen is often problematic to analyze, and insufficient information is available, because it grows slowly and poorly in subculture under a microaerobic atmosphere. The first-choice therapy to eradicate H. cinaedi is antimicrobial chemotherapy; however, its use is linked to the development of resistance. Although we need to understand the antimicrobial resistance mechanisms of H. cinaedi, unfortunately, sufficient genetic tools for H. cinaedi have not yet been developed. In July 2012, the complete sequence of H. cinaedi strain PAGU 611, isolated from a case of human bacteremia, was announced. This strain possesses multidrug efflux systems, intrinsic antimicrobial resistance mechanisms and typical mutations in gyrA and the 23S rRNA gene, which are involved in acquired resistance to fluoroquinolones and macrolides, respectively. Here, we compare the organization and properties of the efflux systems of H. cinaedi with the multidrug efflux systems identified in other bacteria.</jats:p>
収録刊行物
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- Antibiotics
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Antibiotics 1 (1), 29-43, 2012-11-21
MDPI AG
