Antibiotics 2012, 1(1), 29-43; doi:10.3390/antibiotics1010029
Review

Multidrug Efflux Systems in Helicobacter cinaedi

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Received: 29 October 2012; in revised form: 16 November 2012 / Accepted: 16 November 2012 / Published: 21 November 2012
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: 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.
Keywords: Helicobacter cinaedi; efflux; antimicrobial resistance
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MDPI and ACS Style

Morita, Y.; Tomida, J.; Kawamura, Y. Multidrug Efflux Systems in Helicobacter cinaedi. Antibiotics 2012, 1, 29-43.

AMA Style

Morita Y, Tomida J, Kawamura Y. Multidrug Efflux Systems in Helicobacter cinaedi. Antibiotics. 2012; 1(1):29-43.

Chicago/Turabian Style

Morita, Yuji; Tomida, Junko; Kawamura, Yoshiaki. 2012. "Multidrug Efflux Systems in Helicobacter cinaedi." Antibiotics 1, no. 1: 29-43.

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