Resistance

to aminoglycoside antibiotics occurs through a

Resistance

to aminoglycoside antibiotics occurs through a number of mechanisms including enzymatic modification, decreased cellular penetration, active efflux and target site alterations with the former being most common [15]. On that basis, it is reasonable AR-13324 to consider aminoglycoside therapy for infections involving Gram-negative pathogens suspected of producing newer ESBLs or carbapenemases. However, the observation that such bacteria often carry resistance determinants to other antibiotic classes, including aminoglycosides, fluoroquinolones and folic acid inhibitors, may undermine that line of thinking [7–9]. The fact that other broad-spectrum antibiotic exposure may represent a risk factor for acquisition and infection by such organisms only exacerbates the challenge of identifying suitable therapy [16]. The positive aspect of our findings is perhaps that susceptibility of these key Gram-negative pathogens seems to be stable, at least at our institution. This may well be due to low levels of use in comparison with other Gram-negative agents. In fact, tobramycin remains the most active of our routinely tested antibiotics against P. aeruginosa while the vast majority of E. coli and K. pneumoniae are susceptible to amikacin. Thus, the aminoglycosides merit consideration this website in selecting antibiotic therapy for otherwise resistant Gram-negative pathogens. With our current level of understanding

regarding proper aminoglycoside dosing, based upon pharmacodynamics characteristics [12], aminoglycosides Atazanavir represent potentially effective and relatively safe antibiotics. At the same time, it must be noted that a 2009 publication, reporting susceptibility data for a variety of bacteria including our organisms of interest collected and tested from 1999 through 2008, noted increasing aminoglycoside

resistance [17]. That study collected isolates associated with serious infections from hospitals across the United States [17]. While levels of aminoglycoside use cannot be ascertained, that report emphasizes the importance of each hospital determining its own circumstances with regard to aminoglycoside susceptibility patterns [17]. The current study is not without limitations. As this is a single-center analysis, our results cannot be extrapolated to other hospitals or healthcare PF-02341066 datasheet settings. We limited our investigation to P. aeruginosa, E. coli and K. pneumoniae as they are all common causes of healthcare associated infections and are often multidrug resistant [18]. Obviously, a number of other Gram-negative and Gram-positive pathogens are also problematic, multidrug resistant causes of healthcare associated infections and were not considered here. Because we used hospital antibiogram data, there could be an influence of including susceptibilities from both infecting and colonizing organisms on the values, as opposed to only considering organisms associated with documented infections.

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