Relationship of various infection control interventions to the prevalence of multidrug-resistant Pseudomonas aeruginosa among U.S. hospitals

Buford, Victor R.; Kumar, Vibha; Kennedy, Bernice

doi:10.1016/j.ajic.2015.10.033

Cited by 10 publications

(4 citation statements)

References 33 publications

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“…Moreover, it was shown to promote the proliferation of species that have innate resistance to colistin, such as Bulkhorderhia cepaciae , (Cetin et al, 2013). Since these species are considered as highly potent pathogens, they have the potential of causing severe secondary infections following colistin treatment and leave physicians without any viable therapeutic options (Buford et al, 2016; Srinivasan et al, 2016). …”

Section: Discussionmentioning

confidence: 99%

In vitro Evaluation of the Colistin-Carbapenem Combination in Clinical Isolates of A. baumannii Using the Checkerboard, Etest, and Time-Kill Curve Techniques

Soudeiha

Dahdouh

Azar

et al. 2017

Front. Cell. Infect. Microbiol.

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The worldwide increase in the emergence of carbapenem resistant Acinetobacter baumannii (CRAB) calls for the investigation into alternative approaches for treatment. This study aims to evaluate colistin-carbapenem combinations against Acinetobacter spp., in order to potentially reduce the need for high concentrations of antibiotics in therapy. This study was conducted on 100 non-duplicate Acinetobacter isolates that were collected from different patients admitted at Saint George Hospital-University Medical Center in Beirut. The isolates were identified using API 20NE strips, which contain the necessary agents to cover a panel of biochemical tests, and confirmed by PCR amplification of blaOXA−51−like. Activities of colistin, meropenem and imipenem against Acinetobacter isolates were determined by ETEST and microdilution methods, and interpreted according to the guidelines of the Clinical and Laboratory Standards Institute. In addition, PCR amplifications of the most common beta lactamases contributing to carbapenem resistance were performed. Tri locus PCR–typing was also performed to determine the international clonality of the isolates. Checkerboard, ETEST and time kill curves were then performed to determine the effect of the colistin-carbapenem combinations. The synergistic potential of the combination was then determined by calculating the Fractional Inhibitory Concentration Index (FICI), which is an index that indicates additivity, synergism, or antagonism between the antimicrobial agents. In this study, 84% of the isolates were resistant to meropenem, 78% to imipenem, and only one strain was resistant to colistin. 79% of the isolates harbored blaOXA−23−like and pertained to the International Clone II. An additive effect for the colistin-carbapenem combination was observed using all three methods. The combination of colistin-meropenem showed better effects as compared to colistin-imipenem (p < 0.05). The colistin-meropenem and colistin-imipenem combinations also showed a decrease of 2.6 and 2.8-fold, respectively in the MIC of colistin (p < 0.001). Time kill assays additionally showed synergistic effects for a few isolates, and no bacterial re-growth was detected following a 24 h incubation. Our study showed that the combination of colistin with carbapenems could be a promising antimicrobial strategy in treating CRAB infections and potentially lowering colistin toxicity related to higher doses used in colistin monotherapy.

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Section: Discussionmentioning

confidence: 99%

In vitro Evaluation of the Colistin-Carbapenem Combination in Clinical Isolates of A. baumannii Using the Checkerboard, Etest, and Time-Kill Curve Techniques

Soudeiha

Dahdouh

Azar

et al. 2017

Front. Cell. Infect. Microbiol.

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“…Multidrug resistant pathogens are subject of concern because of high fatality rates due to infections in health care settings. The multidrug resistance rates were reported as 59% in E.coli [2], 50% in K.pneumoniae [3], 31.4% in S.epidermidis [4], and 20.6% in P.aeruginosa [5]. Biofilm production of these bacteria also increases the risk of treatment failure.…”

Section: Introductionmentioning

confidence: 99%

Broad spectrum antibacterial photodynamic and photothermal therapy achieved with indocyanine green loaded SPIONs under near infrared irradiation

et al. 2020

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“…The World Health Organization identified it as a critical priority pathogen due to its multi-drug resistance and ability to form biofilms. [1][2][3] Patients with cystic fibrosis are especially susceptible to chronic P. aeruginosa infections; mutations in the cystic fibrosis transmembrane conductance reporter (CFTR) gene produce an environment conducive to infection with P. aeruginosa. 4 Biofilm formation by P. aeruginosa is a major factor in colonization of various surfaces including medical devices and subsequent recalcitrance to treatment, resulting in chronic infections that are very difficult to eradicate.…”

Section: Introductionmentioning

confidence: 99%

A genetic screen identifies a role foroprFinPseudomonas aeruginosabiofilm stimulation by subinhibitory antibiotics

Yaeger,

Ranieri,

Chee

et al. 2023

Preprint

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Biofilms are surface-associated communities of bacteria that grow in a self-produced matrix of polysaccharides, proteins, and extracellular DNA (eDNA). Sub-minimal inhibitory concentrations (sub-MIC) of antibiotics induce biofilm formation, indicating a potential defensive response to antibiotic stress. However, the mechanisms behind sub-MIC antibiotic-induced biofilm formation are unclear. We show that treatment ofPseudomonas aeruginosawith multiple classes of sub-MIC antibiotics with distinct targets induces biofilm formation. Further, addition of exogenous eDNA or cell lysate failed to increase biofilm formation to the same extent as antibiotics, suggesting that the release of cellular contents by antibiotic-driven bacteriolysis is insufficient. Using a genetic screen to find stimulation-deficient mutants, we identified the outer membrane porin OprF and the extracytoplasmic function sigma factor SigX as important for the phenotype. Similarly, loss of OmpA - theEscherichia coliOprF homologue - prevented sub-MIC antibiotic stimulation ofE. colibiofilms. The C-terminal PG-binding domain of OprF was dispensable for biofilm stimulation. Our screen also identified the periplasmic disulfide bond-forming enzyme DsbA and a predicted cyclic-di-GMP phosphodiesterase encoded by PA2200 as essential for biofilm stimulation. The phosphodiesterase activity of PA2200 is likely controlled by a disulfide bond in its regulatory domain, and folding of OprF is influenced by disulfide bond formation, connecting the mutant phenotypes. Addition of the reducing agent dithiothreitol prevented sub-MIC antibiotic biofilm stimulation. Finally, we show that activation of a c-di-GMP-responsive promoter follows treatment with sub-MIC antibiotics in the wild-type but not anoprFmutant. Together, these results show that antibiotic-induced biofilm formation is likely driven by a signalling pathway that translates changes in periplasmic redox state into elevated biofilm formation through increases in c-di-GMP.

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Relationship of various infection control interventions to the prevalence of multidrug-resistant Pseudomonas aeruginosa among U.S. hospitals

Cited by 10 publications

References 33 publications

In vitro Evaluation of the Colistin-Carbapenem Combination in Clinical Isolates of A. baumannii Using the Checkerboard, Etest, and Time-Kill Curve Techniques

In vitro Evaluation of the Colistin-Carbapenem Combination in Clinical Isolates of A. baumannii Using the Checkerboard, Etest, and Time-Kill Curve Techniques

Broad spectrum antibacterial photodynamic and photothermal therapy achieved with indocyanine green loaded SPIONs under near infrared irradiation

A genetic screen identifies a role foroprFinPseudomonas aeruginosabiofilm stimulation by subinhibitory antibiotics

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