Sub-minimum inhibitory concentrations of ceftazidime inhibit Pseudomonas aeruginosa biofilm formation

Otani, Satoshi; Hiramatsu, Kazufumi; Hashinaga, Kazuhiko; Komiya, Kosaku; Umeki, Kenji; Kishi, Kenji; Kadota, Jun‐ichi

doi:10.1016/j.jiac.2018.01.007

Cited by 34 publications

(27 citation statements)

References 29 publications

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“…Noticeably, a 24 h ciprofloxacin exposure induced a deep disruption of the biofilm matrix. It was recently described that the β-lactam ceftazidime may weaken the polysaccharide matrix synthesis of P. aeruginosa PAO1 through a reduction in the production of Pel and Psl exopolysaccharides (Otani et al, 2018). Yasuda et al (1993) also showed that clarithromycin treatment reduced the quantity of alginate and hexose and resulted in eradication of the membranes structures of the biofilm.…”

Section: Discussionmentioning

confidence: 99%

Understanding Ciprofloxacin Failure in Pseudomonas aeruginosa Biofilm: Persister Cells Survive Matrix Disruption

et al. 2019

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Biofilms are commonly recalcitrant to antibiotics, through incompletely elucidated mechanisms such as tolerance and persistence. We aimed at investigating how a Pseudomonas aeruginosa biofilm escapes ciprofloxacin treatment. P. aeruginosa PA14 in vitro mature biofilms were challenged with supra-MIC ciprofloxacin concentrations. Cell viability was quantified by fluorescein diacetate assay. Population dynamics were determined by counts of surviving culturable cells. Biofilms were analyzed using confocal laser scanning microscopy (CLSM), and the expression of genes involved in stringent response, toxin-antitoxin HigB/HigA, and type 3 secretion system (T3SS) was quantified by RT-qPCR in untreated and treated biofilms. Ciprofloxacin exposure resulted in an initial reduction of bacterial counts following a biphasic time-kill curve. After 24 h of treatment, the overall cell activity and the density of culturable cells significantly decreased as compared to untreated biofilm. No resistant mutant was isolated among the <1% surviving cells. Phenotypic adaptation toward persistence appeared to start after only 1 h of antibiotic exposure, by an overexpression of the genes involved in stringent response and in the toxin-antitoxin system, whereas the expression of genes encoding for the T3SS remained unchanged. After 4 h of ciprofloxacin exposure, stringent response genes returned to their basal level of expression. After a prolonged ciprofloxacin exposure, a deep alteration in the matrix structure that became thinner and lost mushroom-like aggregates was observed, in relation with reduced biovolumes of exopolysaccharides and extracellular DNA. These results support that ciprofloxacin might first induce the bacterial killing of most bacterial cells, but simultaneously activate stringent response mechanisms contributing to the switch of a subpopulation toward a persister phenotype. Once the persister phenotype is expressed, and despite an unexpected alteration of the biofilm matrix, ciprofloxacin fails to eradicate biofilm.

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Section: Discussionmentioning

confidence: 99%

Understanding Ciprofloxacin Failure in Pseudomonas aeruginosa Biofilm: Persister Cells Survive Matrix Disruption

et al. 2019

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“…In a recent study, Otani et al (2018) showed that sub-MICs of ceftazidime reduce biofilm volume, inhibit twitching motility, and repress gene expression involved in bacterial adhesion and matrix production of P. aeruginosa PAO1. Roudashti et al (2017) had previously noticed this effect of cephalosporin on motility and biofilm formation for the same strain.…”

Section: Effectiveness Of Conventional Antibioticsmentioning

confidence: 99%

Clinical Impact of Antibiotics for the Treatment of Pseudomonas aeruginosa Biofilm Infections

Olivares

Badel-Berchoux²,

Provot³

et al. 2020

Front. Microbiol.

157

126

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Bacterial biofilms are highly recalcitrant to antibiotic therapies due to multiple tolerance mechanisms. The involvement of Pseudomonas aeruginosa in a wide range of biofilmrelated infections often leads to treatment failures. Indeed, few current antimicrobial molecules are still effective on tolerant sessile cells. In contrast, studies increasingly showed that conventional antibiotics can, at low concentrations, induce a phenotype change in bacteria and consequently, the biofilm formation. Understanding the clinical effects of antimicrobials on biofilm establishment is essential to avoid the use of inappropriate treatments in the case of biofilm infections. This article reviews the current knowledge about bacterial growth within a biofilm and the preventive or inducer impact of standard antimicrobials on its formation by P. aeruginosa. The effect of antibiotics used to treat biofilms of other bacterial species, as Staphylococcus aureus or Escherichia coli, was also briefly mentioned. Finally, it describes two in vitro devices which could potentially be used as antibiotic susceptibility testing for adherent bacteria.

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“…Notably, most of these studies conducted with the final inhibition efficacy of AgNPs, namely, how to obtain the optimal lethal concentration that is toxic to microorganisms but safe for human and environment. Yet, the effects of sublethal concentration of AgNPs exposure on biofilm are poorly understood, which is essential to understand the impacts of AgNPs released from commercial products on microbial ecosystems in the environment or engineered systems . In addition, the biofilm formation is a complex serial process involving surface‐attached planktonic bacteria in the initial stage, the attached cells proliferation and EPS generation, and the mature biofilm with maximum biomass .…”

Section: Introductionmentioning

confidence: 99%

Silver nanoparticles exert concentration‐dependent influences on biofilm development and architecture

et al. 2019

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Objectives:To investigate the impact of silver nanoparticles (AgNPs) on the biofilm growth and architecture.Materials and methods: Silver nitrate was reduced by d-maltose to prepare AgNPs in the presence of ammonia and sodium hydroxide. The physicochemical properties of AgNPs were characterized by transmission electron microscopy, ultraviolet-visible spectroscopy and inductively coupled plasma mass spectrometry. The development of biofilm with and without AgNPs was explored by crystal violet stain. The structures of mature biofilm were visually studied by confocal laser scanning microscopy and scanning electron microscopy. Bacterial cell, polysaccharide and protein within biofilm were assessed quantitatively by colony-counting method, phenol-sulphuric acid method and Bradford assay, respectively. Results:The spherical AgNPs (about 30 nm) were successfully synthesized. The effect of AgNPs on Pseudomonas aeruginosa biofilm development was concentrationdependent. Biofilm was more resistant to AgNPs than planktonic cells. Low doses of AgNPs exposure remarkably delayed the growth cycle of biofilm, whereas high concentration (18 μg/mL) of AgNPs fully prevented biofilm development. The analysis of biofilm architecture at the mature stage demonstrated that AgNPs exposure at all concentration led to significant decrease of cell viability within treated biofilms.However, sublethal doses of AgNPs increased the production of both polysaccharide and protein compared to control, which significantly changed the biofilm structure.Conclusions: AgNPs exert concentration-dependent influences on biofilm development and structure, which provides new insight into the role of concentration played in the interaction between antibacterial nanoparticles and biofilm, especially, an ignored sublethal concentration associated with potential unintended consequences.

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Sub-minimum inhibitory concentrations of ceftazidime inhibit Pseudomonas aeruginosa biofilm formation

Cited by 34 publications

References 29 publications

Understanding Ciprofloxacin Failure in Pseudomonas aeruginosa Biofilm: Persister Cells Survive Matrix Disruption

Understanding Ciprofloxacin Failure in Pseudomonas aeruginosa Biofilm: Persister Cells Survive Matrix Disruption

Clinical Impact of Antibiotics for the Treatment of Pseudomonas aeruginosa Biofilm Infections

Silver nanoparticles exert concentration‐dependent influences on biofilm development and architecture

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