We present Very Large Array (VLA) radio and Chandra X-ray observations of the merging galaxy cluster A3411. For the cluster, we find an overall temperature of 6.4^{}${$+0.6$}$_${$-1.0$}$ keV and... Show moreWe present Very Large Array (VLA) radio and Chandra X-ray observations of the merging galaxy cluster A3411. For the cluster, we find an overall temperature of 6.4^{}${$+0.6$}$_${$-1.0$}$ keV and an X-ray luminosity of 2.8 {plusmn} 0.1 { imes} 10$^{44}$ erg s$^{-1}$ between 0.5 and 2.0 keV. The Chandra observation reveals the cluster to be undergoing a merger event. The VLA observations show the presence of large-scale diffuse emission in the central region of the cluster, which we classify as a 0.9 Mpc size radio halo. In addition, a complex region of diffuse, polarized emission is found in the southeastern outskirts of the cluster along the projected merger axis of the system. We classify this region of diffuse emission as a radio relic. The total extent of this radio relic is 1.9 Mpc. For the combined emission in the cluster region, we find a radio spectral index of -1.0 {plusmn} 0.1 between 74 MHz and 1.4 GHz. The morphology of the radio relic is peculiar, as the relic is broken up into five fragments. This suggests that the shock responsible for the relic has been broken up due to interaction with a large-scale galaxy filament connected to the cluster or other substructures in the intracluster medium. Alternatively, the complex morphology reflects the presence of electrons in fossil radio bubbles that are re-accelerated by a shock. Show less
Background: Antimicrobial use is recognized as a risk factor for Clostridium difficile infection (CDI) and outbreaks. We studied the relationship between PCR ribotype, antimicrobial susceptibility... Show moreBackground: Antimicrobial use is recognized as a risk factor for Clostridium difficile infection (CDI) and outbreaks. We studied the relationship between PCR ribotype, antimicrobial susceptibility and the genetic basis of resistance in response to exposure to antimicrobial agents. Methods: C. difficile isolates were cultured from 133 CDI patients for whom recent antimicrobial drug exposure had been recorded. Isolates were ribotyped by PCR and assessed for their susceptibility to the macrolide-lincosamide-streptogramin B (MLSB) group of compounds (erythromycin and clindamycin) and fluoroquinolone antimicrobials (ciprofloxacin, levofloxacin and moxifloxacin). Where relevant, the genetic basis of resistance was determined. Results: Prevalent ribotypes (including 027, 001 and 106) exhibited significantly greater antimicrobial resistance compared with ribotypes 078 and 014, among others. Clindamycin-resistant ribotype 078 was detected for the first time. Ribotypes 027 and 001 were more likely to exhibit MLSB resistance, a feature that was associated with the erm(B) gene. Exposure to MLSB or fluoroquinolone antimicrobial compounds in the 8 weeks prior to the onset of infection was not associated with specific genetic markers of resistance. Single amino acid substitutions in the A and B subunits of DNA gyrase were noted and were ribotype specific and linked to resistance to moxifloxacin. Conclusions: Resistance to MLSB and fluoroquinolone antimicrobial compounds is common among prevalent ribotypes of C. difficile. The genetic basis for antimicrobial resistance appears to be ribotype specific and conserved in the absence of recent antimicrobial selection pressure. Show less
