Biofilms and Planktonic Cells of Pseudomonas aeruginosa Have Similar Resistance to Killing by Antimicrobials
By Amy Spoering, Kim Lewis. Journal of Bacteriology, 2001
905 citations recorded by the source corpus.
Subfields: Endocrinology, Molecular Biology, Molecular Medicine
View Paper: https://www.semanticscholar.org/paper/1e9c4e7d129e8d32d5304adc777dd5607ac9e9e3
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In Endocrinology
- Kim Lewis
- P. Stoodley
- L. Hall-Stoodley
- P. Watnick
- E. Karatan
- Annelies S. Zinkernagel
- M. Huemer
- S. Brugger
In Molecular Biology
In Molecular Medicine
Citations in the corpus
- Signals, Regulatory Networks, and Materials That Build and Break Bacterial Biofilms (2009, background): “Stationaryphase cells have in fact been shown to be even more tolerant than biofilm cells to some antibiotics (300).”
- Healthcare-associated infections, medical devices and biofilms: risk, tolerance and control. (2015, neutral): “(Spoering & Lewis, 2001; Hall-Stoodley et al., 2004; Lewis, 2008, 2010; Percival et al., 2011).”
- Multidrug tolerance of biofilms and persister cells. (2008, background): “But if biofilms are not resistant, how do they resist being killed? Biofilm resistance to killing has been one of the more elusive problems in microbiology, but the analysis of a simple doseresponse experiment provided an unexpected insight into the puzzle (Brooun et al. 2000; Lewis 2001b; Spoering ”
- Antifungal Susceptibility of Candida Biofilms: Unique Efficacy of Amphotericin B Lipid Formulations and Echinocandins (2002, background): “Whether these cells represent a population of “persisters” (31, 53) remains to be determined.”
- Mechanisms of bacterial persistence during stress and antibiotic exposure (2016, background): “Therefore, the notorious recalcitrance of biofilms to antibiotic treatment and their propensity to relapse have largely been attributed to the high amounts of persisters that form inside a structure (11, 64, 65).”
- Involvement of Nitric Oxide in Biofilm Dispersal of Pseudomonas aeruginosa (2006, background): “Several factors have been suggested to contribute to increased resistance of biofilm cells, including reduced metabolic activity and growth rates of the sessile cells (58), limited antibiotic penetration due to the protective structure of the biofilm (9, 14), and phenotypic diversification of biofil”
- Specialized Persister Cells and the Mechanism of Multidrug Tolerance in Escherichia coli (2004, background): “Only persisters survive under these conditions (28, 44).”
- Extracellular DNA Chelates Cations and Induces Antibiotic Resistance in Pseudomonas aeruginosa Biofilms (2008, background): “Other resistance mechanisms include the presence of subpop ulations of multidrug tolerant persister cells [27–29], drug”
- Bacterial biofilms: from the Natural environment to infectious diseases (2004, background): “The lysing population can be regarded as a third phenotype, whereas the remaining swarming cells might be a surviving, apoptosis-negative, 'persister' phenotyp”
- Contributions of Antibiotic Penetration, Oxygen Limitation, and Low Metabolic Activity to Tolerance of Pseudomonas aeruginosa Biofilms to Ciprofloxacin and Tobramycin (2003, background): “The second explanation is that nutrient limitation leads to slow growth or stationary phase existence for many of the cells in a biofilm, reducing their antimicrobial susceptibility (3, 25).”
- Biofilm-Related Infections: Bridging the Gap between Clinical Management and Fundamental Aspects of Recalcitrance toward Antibiotics (2014, background): “In general, preexposure to subinhibitory concentrations of antibiotics (0.2-fold MIC) increases the frequency of persisters with tolerance toward drugs belonging to different classes of antibiotics (ciprofloxacin, gentamicin, oxacillin, and vancomycin) (180).”
- Antibiotic resistance and persistence—Implications for human health and treatment perspectives (2020, positive): “The group of Kim Lewis was the first to link bacterial persistence to biofilms in P. aeruginosa (Brooun et al , 2000; Spoering & Lewis, 2001).”