However, after patient

However, after patient ErbB2 protein discharge, the strain associated with this patient was never seen again during the course of the study in any location. WGS permits source tracking of P. aeruginosa to individual water outlets WGS has been reported previously for source tracking, but never for the detection of transmission events from hospital water.40 Phylogenetic reconstruction within Clade E, the most commonly detected water clone demonstrated additional diversity within this clone, with a total of 46 mutations detected an average genetic distance between isolates of 4.1 mutations (figure 3). The reconstruction demonstrated clear evidence of clustering of genotypes

both by room and outlet (figure 3). When P. aeruginosa was detected in

the wet environment (eg, shower rosettes and drains) these genotypes were most often identical to those found in water, indicating that the water was likely the ultimate source of that clone. Genotypic variation was seen between outlets within the same room. For example, tap water sampled from room 11 had a distinct genotype from that sampled from shower water in the same room and this was consistently found over multiple samplings. Notably, isolates from two patients fell within the cluster originating from shower water, indicating that shower hydrotherapy was the most likely source of infection. Two plasmids (designated pBURNS1 and pBURNS2) were detected in this study set, which both demonstrated geographical clustering, with pBURNS1 only being detectable in isolates from room 8 and pBURNS2 only being detectable in isolates from the shower water in room 9. FigureĀ 3 The high-resolution phylogenetic reconstruction of Clade E isolates. This demonstrates the clustering of genotypes by bed space. Patient associated samples

are contained within a room 11 clade. This clade contains water samples from the shower and environmental … Rapid evolution of antibiotic resistance associated with treatment P. aeruginosa is commonly associated with antibiotic resistance due to a number of predisposing features including intrinsic resistance, a repertoire of efflux pumps and antibiotic-inactivating Cilengitide enzymes including Ī²-lactamases.41 Three infected patients (2, 3 and 5) received antibiotic therapy, and in each case this was associated with the development of resistance to at least one therapeutic agent. Associated mutations were detected that were either partially or fully explanatory of the phenotype (online supplementary appendix 12). Patient 2 was treated with ciprofloxacin, nitrofurantoin and vancomycin (see online supplementary appendix 11 for full details). Eight of 21 (38%) tested isolates from this patient were ciprofloxacin resistant. Seven of eight isolates (88%) of the ciprofloxacin-resistant strains were distinguishable from the other isolates by a single SNP in mexS (annotated as PA2491 in P.

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