Universidad Complutense de Madrid
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Fluoroquinolone efflux in Streptococcus suis is mediated by SatAB and not by SmrA

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Escudero, Jose Antonio and San Millán, Alvaro and Gutiérrez, Belen and Hidalgo, Laura and La Ragione, Roberto M and AbuOun, Manal and Galimand, Marc and Ferrándiz, María José and Domínguez Rodríguez, Lucas and de la Campa, Adela G and González Zorn, Bruno (2011) Fluoroquinolone efflux in Streptococcus suis is mediated by SatAB and not by SmrA. Antimicrobial agents and chemotherapy, 55 (12). pp. 5850-60. ISSN 1098-6596

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Official URL: http://aac.asm.org/content/55/12/5850.full



Abstract

Streptococcus suis is an emerging zoonotic pathogen. With the lack of an effective vaccine, antibiotics remain the main tool to fight infections caused by this pathogen. We have previously observed a reserpine-sensitive fluoroquinolone (FQ) efflux phenotype in this species. Here, SatAB and SmrA, two pumps belonging to the ATP binding cassette (ABC) and the major facilitator superfamily (MFS), respectively, have been analyzed in the fluoroquinolone-resistant clinical isolate BB1013. Genes encoding these pumps were overexpressed either constitutively or in the presence of ciprofloxacin in this strain. These genes could not be cloned in plasmids in Escherichia coli despite strong expression repression. Finally, site-directed insertion of smrA and satAB in the amy locus of the Bacillus subtilis chromosome using ligated PCR amplicons allowed for the functional expression and study of both pumps. Results showed that SatAB is a narrow-spectrum fluoroquinolone exporter (norfloxacin and ciprofloxacin), susceptible to reserpine, whereas SmrA was not involved in fluoroquinolone resistance. Chromosomal integration in Bacillus is a novel method for studying efflux pumps from Gram-positive bacteria, which enabled us to demonstrate the possible role of SatAB, and not SmrA, in fluoroquinolone efflux in S. suis.


Item Type:Article
Subjects:Medical sciences > Veterinary
ID Code:39677
Deposited On:09 Jan 2017 16:03
Last Modified:09 Jan 2017 16:03

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