Trends in antibiotic resistance over time among pathogens from Canadian hospitals: results of the CANWARD study 2007-11

Lagacé-Wiens, Philippe; Adam, Heather J.; Low, Donald E.; Blondeau, Joseph M; Baxter, Melanie; Denisuik, Andrew; Nichol, Kim; Walkty, Andrew; Karlowsky, James A.; Mulvey, Michael R.; Hoban, Daryl J.; Zhanel, George G.

doi:10.1093/jac/dkt023

Cited by 39 publications

(27 citation statements)

References 32 publications

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“…In Canada and Australia, the prevalence of ESBL phenotypes in E coli has roughly doubled from around only 3% five years ago. [33][34][35] Ciprofloxacin resistance in clinical isolates of E coli increased from 5.4% in 2010 to 6.9% in 2012 in Australia, and from 21% to 27% between 2007 and 2011 in Canada, where fluoroquinolone usage has been somewhat higher than in Australia. 33 Fig 1 | Timeline of bacterial evolution.…”

Section: Incidence and Prevalencementioning

confidence: 99%

“…[33][34][35] Ciprofloxacin resistance in clinical isolates of E coli increased from 5.4% in 2010 to 6.9% in 2012 in Australia, and from 21% to 27% between 2007 and 2011 in Canada, where fluoroquinolone usage has been somewhat higher than in Australia. 33 Fig 1 | Timeline of bacterial evolution. The introduction of each antibiotic has been quickly followed by recognition of an adaptation (including a phenotype or mechanism, as marked on resistance timeline) to resist it.…”

Section: Incidence and Prevalencementioning

confidence: 99%

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Antibiotic resistance in Enterobacteriaceae: mechanisms and clinical implications

Iredell

Brown

Tagg

2016

BMJ

289

177

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Resistance of the Enterobacteriaceae to antibiotics, especially of the β lactam type, is increasingly dominated by the mobilization of continuously expressed single genes that encode efficient drug modifying enzymes. Strong and ubiquitous selection pressure has seemingly been accompanied by a shift from "natural" resistance, such as inducible chromosomal enzymes, membrane impermeability, and drug efflux, to the modern paradigm of mobile gene pools that largely determine the epidemiology of modern antibiotic resistance. In this way, antibiotic resistance is more available than ever before to organisms such as Escherichia coli and Klebsiella pneumoniae that are important causes of major sepsis. Modulation of the phenotype by host bacteria makes gene transmission less obvious and may in part explain why tracking and control of carbapenem resistance has been particularly problematic in the Enterobacteriaceae. This review discusses the underlying principles and clinical implications of the mobility and fixation of resistance genes and the exploitable opportunities and potential threats arising from apparent limitations on diversity in these mobile gene pools. It also provides some illustrative paradoxes and clinical corollaries, as well as a summary of future options.

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Section: Incidence and Prevalencementioning

confidence: 99%

Section: Incidence and Prevalencementioning

confidence: 99%

Antibiotic resistance in Enterobacteriaceae: mechanisms and clinical implications

Iredell

Brown

Tagg

2016

BMJ

289

177

View full text Add to dashboard Cite

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“…Although a North America study it should be noted that the majority of North American sites in SMART are located in the US. The CAN-WARD study of Canadian hospitals reported a statistically significant (p < 0.001) decrease in fluoroquinolone (ciprofloxacin) resistance among P. aeruginosa between 2007 and 2011, from 34.0 to 21.8% [17]. However, the isolates in the Lagac eWiens et al study were not solely from IAIs [17].…”

Section: Drug Name (Generic)mentioning

confidence: 88%

“…The CAN-WARD study of Canadian hospitals reported a statistically significant (p < 0.001) decrease in fluoroquinolone (ciprofloxacin) resistance among P. aeruginosa between 2007 and 2011, from 34.0 to 21.8% [17]. However, the isolates in the Lagac eWiens et al study were not solely from IAIs [17]. In their surveillance study of isolates collected from IAIs from US medical centers in 2012, Flamm et al reported that 10.4% of E. coli and 16.3% of Klebsiella spp.…”

Section: Drug Name (Generic)mentioning

confidence: 99%

Focus on ceftazidime-avibactam for optimizing outcomes in complicated intra-abdominal and urinary tract infections

Nicolau

2015

Expert Opinion on Investigational Drugs

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The increasing problem and complexity of β-lactamase resistance has been met by resurgence in the development of β-lactamase inhibitor combinations. These show promise in the treatment of resistant infections. One β-lactamase inhibitor in advanced development with a broad spectrum of activity is avibactam, covering class A, class C and some class D enzymes. Importantly, the activity of avibactam also includes carbapenemases such as the KPC and OXA-48. The combination of avibactam with the cephalosporin ceftazidime is attractive, given the spectrum of antimicrobial activity and the low toxicity of the cephalosporin class.

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“…The emergence of bacterial infections resilient to the current arsenal of antibiotics is increasing (Lagace-Wiens et al, 2013;Spellberg et al, 2008;Zhanel et al, 2013), and the challenge in managing this crisis is that the emergence of antimicrobial multiresistant bacteria is a natural process that relies on both the evolutionary changes and the biological components of the microorganisms. These natural processes, which include gene acquisition, transfer and gene expression, provide the organisms with the ability to adapt and evolve within their environments.…”

Section: The Problem Of Antibiotic Resistancementioning

confidence: 99%

Genomic tools to profile antibiotic mode of action

Cardona

Selin

Gislason

2014

Critical Reviews in Microbiology

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The increasing emergence of antimicrobial multiresistant bacteria is of great concern to public health. While these bacteria are becoming an ever more prominent cause of nosocomial and community-acquired infections worldwide, the antibiotic discovery pipeline has been stalled in the last few years with very few efforts in the research and development of novel antibacterial therapies. Some of the root causes that have hampered current antibiotic drug development are the lack of understanding of the mode of action (MOA) of novel antibiotic molecules and the poor characterization of the bacterial physiological response to antibiotics that ultimately causes resistance. Here, we review how bacterial genetic tools can be applied at the genomic level with the goal of profiling resistance to antibiotics and elucidating antibiotic MOAs. Specifically, we highlight how chemical genomic detection of the MOA of novel antibiotic molecules and antibiotic profiling by next-generation sequencing are leveraging basic antibiotic research to unprecedented levels with great opportunities for knowledge translation.

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Trends in antibiotic resistance over time among pathogens from Canadian hospitals: results of the CANWARD study 2007-11

Cited by 39 publications

References 32 publications

Antibiotic resistance in Enterobacteriaceae: mechanisms and clinical implications

Antibiotic resistance in Enterobacteriaceae: mechanisms and clinical implications

Focus on ceftazidime-avibactam for optimizing outcomes in complicated intra-abdominal and urinary tract infections

Genomic tools to profile antibiotic mode of action

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