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Linezolid is an important last-resort antibiotic for the treatment of multidrug-resistant enterococci. The aim of this study was to further characterize the genetic context of optrA and poxtA in 10 florfenicol-resistant enterococci isolated from flowing surface water. In most genomes, optrA and poxtA were embedded in transposition units integrated into plasmids or into the chromosomal radC . For the first time, a chromosomally integrated optrA in an Enterococcus raffinosus isolate is described.

Linezolid is an important last-resort antibiotic for the treatment of multidrug-resistant enterococci. The aim of this study was to further characterize the genetic context of optrA and poxtA in 10 florfenicol-resistant enterococci isolated from flowing surface water. In most genomes, optrA and poxtA were embedded in transposition units integrated into plasmids or into the chromosomal radC. For the first time, a chromosomally integrated optrA in an Enterococcus raffinosus isolate is described.

Human isolates of Salmonella enterica serovars Hadar, Kentucky, Virchow, Schwarzengrund, and the monophasic variant of S . Typhimurium, Salmonella enterica subsp. enterica serovar 4,5,12:i:− were examined for mutations within the quinolone resistance target genes gyrA , gyrB , parC , and parE and for plasmid-mediated resistance genes. Differences were observed among the serovars. A novel variant of qnrD , qnrD2 , was detected in an S . Hadar isolate.

There is growing evidence that Enterobacteriaceae harboring clinically relevant bla genes, especially genes encoding the CTX-M family of ESBLs, have spread into the environment (1).…

Human isolates of Salmonella enterica serovars Hadar, Kentucky, Virchow, Schwarzengrund, and the monophasic variant of S. Typhimurium, Salmonella enterica subsp. enterica serovar 4,5,12:i:− were examined for mutations within the quinolone resistance target genes gyrA, gyrB, parC, and parE and for plasmid-mediated resistance genes. Differences were observed among the serovars. A novel variant of qnrD, qnrD2, was detected in an S. Hadar isolate.

We developed a system based on site-directed mutagenesis that allows a precise comparison of SHV enzymes under isogenic conditions. In addition, the influences of two different, naturally occurring promoters were examined for each SHV derivative. The system comprised two separately cloned DNA fragments, each the size of 3.6 kb. Both fragments encoded an SHV gene originating from clinical isolates but with different promoters. The structural genes were made identical by site-directed mutagenesis. Other mutations were then introduced into both fragments by means of site-directed mutagenesis, resulting in the SHV derivatives SHV-1, SHV-2, SHV-2a, SHV-3, and SHV-5. The amino acid exchange of glutamic acid at position 235 for lysine in SHV-5 resulted in the highest resistance levels. SHV-3, differing from SHV-2 by the exchange of arginine at position 201 for leucine and previously described as indistinguishable from SHV-2, was shown to cause slightly higher resistance to ceftazidime and lower resistance to ceftriaxone, cefotaxime, and cefepime than SHV-2. The point mutation in SHV-2a, with the leucine-to-glutamine replacement at the unusual position 31, previously considered almost insignificant, proved to increase resistance to ceftazidime but reduced the MICs of all other cephalosporins tested when compared with those for SHV-2. For all clones harboring SHV derivatives, resistance was increased by a stronger promoter, in some cases masking the effect of the point mutation itself and demonstrating the importance of regulatory mechanisms of resistance.

Sixty isolates of Enterobacteriaceae resistant to beta-lactam antibiotics were collected over a period of 2 years in Switzerland and screened by hybridization for the carriage of SHV genes. Thirty-four positive strains were found, and their SHV genes were amplified and sequenced. SHV extended-spectrum beta-lactamases (ESBLs) were found: 13 strains contained SHV-2a, 12 harbored SHV-2, and SHV-5 was found twice. Four strains were shown to contain SHV-1. In addition, we report two new SHV variants, termed SHV-11 (non-ESBL) and SHV-12 (ESBL). In spite of the carriage of SHV ESBLs, many strains showed only low resistance to one or more third-generation cephalosporins. In addition, 26 did not transfer the blaSHV gene in mating experiments.