Ecological theory suggests that antimicrobial cycling will not reduce antimicrobial resistance in hospitals

Bergstrom, Carl T.; Lo, Monique; Lipsitch, Marc

doi:10.1073/pnas.0402298101

Cited by 332 publications

(344 citation statements)

References 38 publications

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“…Furthermore, the frequency with which to rotate antibiotics remains unclear, as monthly and quarterly regimens have been assessed with documented successes (75,165). Furthermore, the probability of antibiotic cycling leading to a reduction in antimicrobial resistance is low as determined through mathematical modeling (14). At this juncture, it is premature to recommend rotating antibiotics or a rotational schema.…”

Section: Preventing Multidrug Resistancementioning

confidence: 99%

Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention

2006

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SUMMARY While critically ill patients experience a life-threatening illness, they commonly contract ventilator-associated pneumonia. This nosocomial infection increases morbidity and likely mortality as well as the cost of health care. This article reviews the literature with regard to diagnosis, treatment, and prevention. It provides conclusions that can be implemented in practice as well as an algorithm for the bedside clinician and also focuses on the controversies with regard to diagnostic tools and approaches, treatment plans, and prevention strategies.

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Section: Preventing Multidrug Resistancementioning

confidence: 99%

Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention

2006

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“…In response to the rise of antibiotic resistance, the continued development of new drugs and the judicious use of our current arsenal of antibiotics is required (Bergstrom et al, 2004). In this context, the development and use of QSinhibition-based drugs to attenuate bacterial pathogenicity is attractive (Boyen et al, 2009;Jones et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Screening for novel quorum-sensing inhibitors to interfere with the formation of Pseudomonas aeruginosa biofilm

Ding

Yin

et al. 2011

Journal of Medical Microbiology

126

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The objective of this study was to screen for novel quorum-sensing inhibitors (QSIs) from traditional Chinese medicines (TCMs) that inhibit bacterial biofilm formation. Six of 46 active components found in TCMs were identified as putative QSIs based on molecular docking studies. Of these, three compounds inhibited biofilm formation by Pseudomonas aeruginosa and Stenotrophomonas maltophilia at a concentration of 200 mM. A fourth compound (emodin) significantly inhibited biofilm formation at 20 mM and induced proteolysis of the quorum-sensing signal receptor TraR in Escherichia coli at a concentration of 3-30 mM. Emodin also increased the activity of ampicillin against P. aeruginosa. Therefore, emodin might be suitable for development into an antivirulence and antibacterial agent. INTRODUCTIONPseudomonas aeruginosa, an opportunistic human pathogen, may cause acute infections in hospitalized patients, can be isolated from the environment, particularly from soil and water, and it regularly contaminates medical devices (Stover et al., 2000). It is also the predominant cause of chronic lung infection in cystic fibrosis patients (Frederiksen et al., 1997) and has recently been recognized as one of the main causes of chronic wound infections (Gjødsbøl et al., 2006). P. aeruginosa can infect patients by producing a wide range of virulence factors, the expression levels of which are tightly regulated. Key to this regulation is cell density-dependent cell-to-cell signalling, which is termed quorum sensing (QS) (Rumbaugh et al., 2000). As in many other bacteria, QS controls secretion of virulence factors (Mittal et al., 2006), biofilm formation (Waters et al., 2008) and the exchange of DNA (Fuqua & Winans, 1996) in P. aeruginosa. The biofilm mode of growth is recognized as an important bacterial trait that is relevant to infections (Costerton et al., 1994). Many infections involve the formation of bacterial biofilms, which are bacterial communities that settle and proliferate on surfaces and are covered by exopolymers (Lewis, 2007). Once established, biofilms are difficult to eradicate and become a source of secondary infection (Jones et al., 2009). Moreover, bacteria embedded in biofilms are more tolerant than planktonic cells of antibiotics (Donlan & Costerton, 2002;Drenkard, 2003). The dose of antibiotics needed in this situation will often exceed the highest deliverable dose, which makes efficient treatment impossible.QS, as a regulatory mechanism, enables bacteria to make collective decisions with respect to the expression of a specific set of genes that involve the production, release and subsequent detection of chemical signalling molecules, such as N-acylhomoserine lactones (AHLs) that are commonly used by Gram-negative bacteria. When the concentration of AHLs reaches a certain threshold level, binding to a receptor molecule (for example, LuxR) is promoted and the activated LuxR-AHL complex forms dimers or polymers, which, in turn, act as transcriptional regulators of target genes in the QS regulon (Parsek & Greenbe...

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“…Hitherto, investigation and policy development for the control of AMR using surveillance data have focused largely on patterns of resistance to individual antimicrobials [4,5]. Quantitative studies have concentrated on theoretical frameworks using simulated and in vitro experimental data [6][7][8], while much of our current understanding of the impacts of individual antimicrobials has been derived from small scale clinical epidemiological studies [9,10].…”

Section: Introductionmentioning

confidence: 99%

An ecological approach to assessing the epidemiology of antimicrobial resistance in animal and human populations

et al. 2011

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We examined long-term surveillance data on antimicrobial resistance (AMR) in Salmonella Typhimurium DT104 (DT104) isolates from concurrently sampled and sympatric human and animal populations in Scotland. Using novel ecological and epidemiological approaches to examine diversity, and phenotypic and temporal relatedness of the resistance profiles, we assessed the more probable source of resistance of these two populations. The ecological diversity of AMR phenotypes was significantly greater in human isolates than in animal isolates, at the resolution of both sample and population. Of 5200 isolates, there were 65 resistance phenotypes, 13 unique to animals, 30 unique to humans and 22 were common to both. Of these 22, 11 were identified first in the human isolates, whereas only five were identified first in the animal isolates. We conclude that, while ecologically connected, animals and humans have distinguishable DT104 communities, differing in prevalence, linkage and diversity. Furthermore, we infer that the sympatric animal population is unlikely to be the major source of resistance diversity for humans. This suggests that current policy emphasis on restricting antimicrobial use in domestic animals may be overly simplistic. While these conclusions pertain to DT104 in Scotland, this approach could be applied to AMR in other bacteria-host ecosystems.

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Ecological theory suggests that antimicrobial cycling will not reduce antimicrobial resistance in hospitals

Cited by 332 publications

References 38 publications

Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention

Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention

Screening for novel quorum-sensing inhibitors to interfere with the formation of Pseudomonas aeruginosa biofilm

An ecological approach to assessing the epidemiology of antimicrobial resistance in animal and human populations

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