Streptococcus Suis is an important zoonotic pathogen and is gaining attention due to emergence of drug resistance and recently reported some deaths of human by this pathogen.  Recently, fluoroquinolone (FQ) resistant strains of Streptococcus suis in animal as well as in human clinics are increasingly reported worldwide. Up to now no study on role of efflux pumps in FQs resistance has been documented, therefore we analyzed resistance mechanisms for FQs in stepwise induced mutants of S. suis strains. Results showed some resistant strains without alterations within QRDR of DNA gyrase enzyme and topoisomerase IV but with a FQs-resistant phenotype. MIC of ciprofloxacin, not enrofloxacin against resistant isolates can be reduced by adding reserpine. It suggests that there were any efflux pumps contributed to ciprofloxacin resistance in S. suis. Furthermore, growth inhibition assays and its parallel assays were performed and the results intensively indicated there are any efflux pumps in ciprofloxacin resistant strains. Based on the high homology of SatA, SatB and SmrA with PatA, PatB and PmrA, which mediated resistance to FQs in Streptococcus pneumococcus, thus the mRNA expression level of satA, saB and smrAwere investigated. Overexpression of satA and satB was found in ciprofloxacin-resistant isolates but expression levels of smrA were not significantly changed in resistant strains if compared with their parental sensitive strains. In addition, isolates overexpressing satA and satB accumulate significantly less ciprofloxacin. In conclusion, all these data represent that SatA and SatB, not SmrA play a clinically relevant role in ciprofloxacin resistance.

Key words: ABC transporters, Efflux pump, Fluoroquinolone resistance, S suis