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Carl F. Marrs 1 Article
Efflux-mediated resistance identified among norfloxacin resistant clinical strains of group B Streptococcus from South Korea
Trang Nguyen Doan Dang, Usha Srinivasan, Zachary Britt, Carl F. Marrs, Lixin Zhang, Moran Ki, Betsy Foxman
Epidemiol Health. 2014;36:e2014022.   Published online October 11, 2014
DOI: https://doi.org/10.4178/epih/e2014022
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  • 6 Citations
AbstractAbstract PDF
Abstract
OBJECTIVES
Group B Streptococcus (GBS), a common bowel commensal, is a major cause of neonatal sepsis and an emerging cause of infection in immune-compromised adult populations. Fluoroquinolones are used to treat GBS infections in those allergic to beta-lactams, but GBS are increasingly resistant to fluoroquinolones. Fluoroquinolone resistance has been previously attributed to quinolone resistance determining regions (QRDRs) mutations. We demonstrate that some of fluoroquinolone resistance is due to efflux-mediated resistance.
METHODS
We tested 20 GBS strains resistant only to norfloxacin with no mutations in the QRDRs, for the efflux phenotype using norfloxacin and ethidium bromide as substrates in the presence of the efflux inhibitor reserpine. Also tested were 68 GBS strains resistant only to norfloxacin not screened for QRDRs, and 58 GBS strains resistant to ciprofloxacin, levofloxacin or moxifloxacin. Isolates were randomly selected from 221 pregnant women (35-37 weeks of gestation) asymptomatically carrying GBS, and 838 patients with GBS infection identified in South Korea between 2006 and 2008. The VITEK II automatic system (Biomerieux, Durham, NC, USA) was used to determine fluoroquinolone resistance.
RESULTS
The reserpine associated efflux phenotype was found in more than half of GBS strains resistant only to norfloxacin with no QRDR mutations, and half where QRDR mutations were unknown. No evidence of the efflux phenotype was detected in GBS strains that were resistant to moxifloxacin or levofloxacin or both. The reserpine sensitive efflux phenotype resulted in moderate increases in norfloxacin minimum inhibitory concentration (average=3.6 fold, range=>1-16 fold).
CONCLUSIONS
A substantial portion of GBS strains resistant to norfloxacin have an efflux phenotype.
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Citations

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  • A review of antibiotic resistance in Group B Streptococcus: the story so far
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    Cinthia Alves-Barroco, Lorenzo Rivas-García, Alexandra R. Fernandes, Pedro Viana Baptista
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  • Fluoroquinolone-Resistant Streptococcus agalactiae Invasive Isolates Recovered in Argentina
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    Microbial Drug Resistance.2019; 25(5): 739.     CrossRef
  • Multidrug efflux pumps of Gram-positive bacteria
    Bryan D. Schindler, Glenn W. Kaatz
    Drug Resistance Updates.2016; 27: 1.     CrossRef
  • Fluoroquinolone Resistance among Clonal Complex 1 Group BStreptococcusStrains
    Alefiya Neemuchwala, Sarah Teatero, Samir N. Patel, Nahuel Fittipaldi
    Canadian Journal of Infectious Diseases and Medical Microbiology.2016; 2016: 1.     CrossRef
  • Molecular Analysis of Rising Fluoroquinolone Resistance in Belgian Non-Invasive Streptococcus pneumoniae Isolates (1995-2014)
    Pieter-Jan Ceyssens, Françoise Van Bambeke, Wesley Mattheus, Sophie Bertrand, Frédéric Fux, Eddie Van Bossuyt, Sabrina Damée, Henry-Jean Nyssen, Stéphane De Craeye, Jan Verhaegen, Paul M. Tulkens, Raymond Vanhoof, Eliane Namie Miyaji
    PLOS ONE.2016; 11(5): e0154816.     CrossRef

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