Revealed similar antibiotic substrate profiles and

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revealed similar antibiotic substrate profiles and activity as the MPH encoded by the mphE gene in B. paraconglomeratum , with no aminoglycoside modification activity (Table 4). Figure 3. MIC of antibiotics determined in this study. Heat Plot for (A) Gram-positive strains (B) Gram-negative strains against various antibiotics. Antibiotics are grouped according to their mode of action and the gradient from light blue to dark blue represents the range from lowest MIC value (0.3 m g/ml) to highest MIC value (256 m g/ml) as shown in the legend. White means no MIC was determined. doi:10.1371/journal.pone.0034953.g003 Table 1. Summary of Antibiotic Inactivation Studies for Gram-positive Isolates. Antibiotic Resistant Strains Number of antibiotic Inactivation Strains Mechanism of Inactivation Apramycin 7 0 ------- Gentamicin 5 0 ------- Neomycin 8 0 ------- Streptomycin 8 0 ------- Tetracycline 4 0 ------- Minocycline 1 0 ------- Clindamycin 6 0 ------- Chloramphenicol 12 0 ------- Synercid 2 0 ------- Erythromycin 7 1 Phosphorylation Telithromycin 4 4 Phosphorylation Glycosylation Linezolid 2 0 ------- Novobiocin 5 0 ------- Cephalexin 17 5 Hydrolysis Ampicillin 8 5 Hydrolysis Piperacillin 9 2 Hydrolysis Daptomycin 24 7 Hydrolysis Strains were grown in 50% TSB for 5 days in presence of 20 m g/ml antibiotic. Conditional media was used for setting up disk diffusion assays and LC-MS analyses. Inactivation was defined as the absence of a zone of clearance around the disk. Hydrolytic mechanism of ß-lactam resistance is inferred. doi:10.1371/journal.pone.0034953.t001 Antibiotic Resistance in Cave Bacteria PLoS ONE | 5 April 2012 | Volume 7 | Issue 4 | e34953
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The mph genes in both Brachybacterium species are organized on comparable regions of the chromosome and flanked by similar genes and synteny (Figure 6); a survey 10 kb upstream and downstream of mph revealed eleven common and five different genes (Figure 6) and the gene products were 75–80% similar. Phylogenetic analysis shows that MPHs from Brachybacterium strains cluster together as a separate group among the known and putative members of the MPH family (Figure S5). Discussion Antibiotic resistance is manifested through a number of different mechanisms including target alteration, control of drug influx and efflux, and through highly efficient enzyme-mediated inactivation. Resistance can emerge relatively quickly in the case of some mutations in target genes and there is evidence that antibiotics themselves can promote such mutations [43,44,45,46]; however, resistance to most antibiotics occurs through the aegis of extremely efficient enzymes, efflux proteins and other transport systems that often are highly specialized towards specific antibiotic molecules. Such elements are the result of evolution through natural selection; this therefore implies that antibiotic resistance has a long evolutionary past. A growing body of evidence suggests that non-pathogenic environmental organisms are a reservoir of resistance genes that have the potential to be transferred to pathogens [31,47,48]. The problem of antibiotic resistance in clinical settings therefore likely has its origins in the environment.
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