S. Tubiana). y Bruno Hoen and Xavier Duval contributed equally. z The members of COMBAT study group are listed at the Acknowledgments section. Contents lists available at ScienceDirect Clinical Microbiology and Infectionj o u r n a l h o m e p a g e : w w w . c l i n i c a l m i c r o b i o l o g y a n d i n f e c t i o n . c o m

qnr genes are plasmid-mediated quinolone resistance genes mainly harbored on large conjugative multiresistant plasmids. The qnrD gene was recently observed in Salmonella enterica on a small nonconjugative plasmid (p2007057). We describe two strains of Providencia rettgeri harboring qnrD on nonconjugative plasmids. The plasmids were 99% identical, with 2,683 bp and four open reading frames, including qnrD, but exhibited only 53% identity with the plasmid found in S. enterica. The first qnr gene was observed in the late 1990s and described as a plasmid-mediated quinolone resistance gene (PMQR). Since then, five types of qnr genes have been reported: qnrA, qnrB, qnrC, qnrD, and qnrS. Their sequences are deposited at the following website (http://www.lahey.org/qnrStudies/). Most were observed in Enterobacteriaceae, located on large conjugative multiresistance plasmids, such as pMG252 seen in the original qnrA1-positive strain (14). qnrD was recently reported in four Salmonella enterica isolates (7) and one Escherichia coli isolate (22). In S. enterica, the gene was located on a small nonconjugative plasmid of 4,270 bp (p2007057), a location greatly different from that of the other qnr genes. We describe two clinical isolates of Providencia rettgeri harboring qnrD. We investigated the genetic support for qnrD in these two strains and showed that qnrD was harbored on a small nonconjugative plasmid which was unlike that found in the Salmonella isolates.P. rettgeri DIJ09-518 was isolated from a stool specimen of a patient admitted in 2008 to the hematology ward of the university hospital in Dijon, France. P. rettgeri GHS09-09 was isolated from three urine specimens of a patient hospitalized in 2009 in the emergency unit at Hôpital Pitié-Salpétrière (Paris, France). Quinolone susceptibility phenotypes are shown in Table 1. bla CTX-M-15 was detected in DIJ09-518. Random amplification of polymorphic DNA confirmed that the two isolates were non-clonally related strains (4). qnrD was detected by using real-time PCR (10). No transconjugant was obtained by either liquid or filter matingout assays with the following recipient strains and selection conditions: sodium azide-resistant E. coli J53, Proteus mirabilis ATCC 29906 Rif r (8), and E. coli C600 Rif r selected on brain heart infusion agar plates containing sodium azide (100 g/ml) or rifampin (250 g/ml) and cefpirome (0.25 g/ml) or ampicillin (100 g/ ml) or nalidixic acid (50 g/ml) or ciprofloxacin (0.03 g/ml and 0.06 g/ml) (12).Southern blot hybridization studies with plasmid DNA extracts showed that qnrD was present on a small (about 2.5 kb) plasmid in the two strains (data not shown). After electroporation of the plasmid DNA extracts and selection on brain heart infusion (BHI) agar plates containing 0.06 g/ml ciprofloxacin, two transformants harboring qnrD were obtained, E. coli DH10B/pDIJ09-518a and E. coli DH10B/pGHS09-09a.Etest data were interpreted by following the EUCAST guidelines (http://www.eucast.org). The MICs of fluoroquinolones for the two transformants were ...

Introduction:We aimed to describe patients with coexisting infective endocarditis (IE) and bacterial meningitis (BM). Methods: We merged two large prospective cohorts, an IE cohort and a BM cohort, with only cases of definite IE and community-acquired meningitis. We compared patients who had IE and BM concurrently to patients with IE only and BM only. Results: Among the 1030 included patients, we identified 42 patients with IE-BM (4.1%). Baseline characteristics of patients with IE-BM were mostly similar to those of patients with IE, but meningitis was the predominant presentation at admission (39/42, 92.3%). Causative pathogens were predominantly Streptococcus pneumoniae (18/42, 42.9%) and Staphylococcus aureus (14/42, 33.3%). All pneumococcal IE were associated with BM (18/18). BM due to oral and group D streptococci, Streptococcus agalactiae, and S. aureus were frequently associated with IE Bruno Hoen and Xavier Duval contributed equally.The members of the AEPEI and the COMBAT study groups are listed in the Acknowledgements section.G. Be ´raud (&)

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