The endotracheal tube microbiome associated with Pseudomonas aeruginosa or Staphylococcus epidermidis

Hotterbeekx, An; Xavier, Basil Britto; Bielen, Kenny; Lammens, Christine; Moons, Pieter; Schepens, Tom; Ieven, Margareta; Jorens, Philippe G.; Goossens, Herman; Kumar‐Singh, Samir; Malhotra-Kumar, Surbhi

doi:10.1038/srep36507

Cited by 50 publications

(49 citation statements)

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“…S. aureus mostly resides on the wound surface whereas P. aeruginosa is found in the deep layers (Kirketerp-Moller et al, 2008; Fazli et al, 2009). We also recently showed a negative correlation between presence of P. aeruginosa and the total species diversity in in vivo endotracheal tube biofilms and a low co-occurrence of P. aeruginosa with Staphylococcus epidermidis (Hotterbeekx et al, 2016). Nonetheless, recent studies have also co-isolated P. aeruginosa and Gram-positive bacteria, including S. aureus , from the same infection site where increased virulence and/or antibiotic resistance is described (Duan et al, 2003; Kirketerp-Moller et al, 2008; Fazli et al, 2009; Dalton et al, 2011; Korgaonkar et al, 2013).…”

Section: Introductionmentioning

confidence: 87%

In vivo and In vitro Interactions between Pseudomonas aeruginosa and Staphylococcus spp.

Hotterbeekx

Kumar‐Singh

Goossens

et al. 2017

Front. Cell. Infect. Microbiol.

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194

249

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The significance of polymicrobial infections is increasingly being recognized especially in a biofilm context wherein multiple bacterial species—including both potential pathogens and members of the commensal flora—communicate, cooperate, and compete with each other. Two important bacterial pathogens that have developed a complex network of evasion, counter-inhibition, and subjugation in their battle for space and nutrients are Pseudomonas aeruginosa and Staphylococcus aureus. Their strain- and environment-specific interactions, for instance in the cystic fibrosis lung or in wound infections, show severe competition that is generally linked to worse patient outcomes. For instance, the extracellular factors secreted by P. aeruginosa have been shown to subjugate S. aureus to persist as small colony variants (SCVs). On the other hand, data also exist where S. aureus inhibits biofilm formation by P. aeruginosa but also protects the pathogen by inhibiting its phagocytosis. Interestingly, such interspecies interactions differ between the planktonic and biofilm phenotype, with the extracellular matrix components of the latter likely being a key, and largely underexplored, influence. This review attempts to understand the complex relationship between P. aeruginosa and Staphylococcus spp., focusing on S. aureus, that not only is interesting from the bacterial evolution point of view, but also has important consequences for our understanding of the disease pathogenesis for better patient management.

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Section: Introductionmentioning

confidence: 87%

In vivo and In vitro Interactions between Pseudomonas aeruginosa and Staphylococcus spp.

Hotterbeekx

Kumar‐Singh

Goossens

et al. 2017

Front. Cell. Infect. Microbiol.

Self Cite

194

249

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“…This biofilm protects bacteria from host immune cells and antibiotics by encapsulation and sequestration (24,25) and thus co-induces the typically persistent type of lung inflammation observed in CF patients (26). Moreover, VAP pathogenesis is also closely linked to biofilm forming organisms colonizing the endotracheal tube (ETT) such as P. aeruginosa, and the presence of P. aeruginosa in the biofilm on the ETT microbiome negatively correlates with patient prognosis (27).…”

Section: Etiology Of Hospital Acquired Pneumoniamentioning

confidence: 99%

Animal models of hospital-acquired pneumonia: current practices and future perspectives

Bielen¹,

Jongers²,

Malhotra-Kumar³

et al. 2017

Ann. Transl. Med.

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Lower respiratory tract infections are amongst the leading causes of mortality and morbidity worldwide. Especially in hospital settings and more particularly in critically ill ventilated patients, nosocomial pneumonia is one of the most serious infectious complications frequently caused by opportunistic pathogens.Pseudomonas aeruginosa is one of the most important causes of ventilator-associated pneumonia as well as the major cause of chronic pneumonia in cystic fibrosis patients. Animal models of pneumonia allow us to investigate distinct types of pneumonia at various disease stages, studies that are not possible in patients.Different animal models of pneumonia such as one-hit acute pneumonia models, ventilator-associated pneumonia models and biofilm pneumonia models associated with cystic fibrosis have been extensively studied and have considerably aided our understanding of disease pathogenesis and testing and developing new treatment strategies. The present review aims to guide investigators in choosing appropriate animal pneumonia models by describing and comparing the relevant characteristics of each model using P. aeruginosa as a model etiology for hospital-acquired pneumonia. Key to establishing and studying these animal models of infection are well-defined end-points that allow precise monitoring and characterization of disease development that could ultimately aid in translating these findings to patient populations in order to guide therapy. In this respect, and discussed here, is the development of humanized animal models of bacterial pneumonia that could offer unique advantages to study bacterial virulence factor expression and host cytokine production for translational purposes.

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“…Despite of known antagonistic interactions between S. aureus and P. aeruginosa 35 , they are still the most common pathogens evoking wound infections and forming mixed biofilms on their surfaces 39,40,42 . We have simulated in vitro different situations where either S. aureus suspension was added to the preformed 24-h old biofilm of P. aeruginosa or, vice versa, P. aeruginosa was added to the preformed 24-h old biofilm of S. aureus .…”

Section: Resultsmentioning

confidence: 99%

“…P. aeruginosa was shown to reduce S. aureus during co-culture in vitro in both planktonic and biofilm forms 30–33 and has been observed as the dominant pathogen in S. aureus-P. aeruginosa mixed infections 16 . Nevertheless, despite of the antagonistic relationship of S. aureus and P. aeruginosa 34,35 , several studies reported their mutual association both in vitro 36,37 and in acute and chronic wounds embedded in a mixed biofilm 8,38–42 , with S. aureus typically residing on the wound surface, whereas P. aeruginosa being rather observed in the deep layers 15,42–45 . Interestingly, in mixed P. aeruginosa - S. aureus biofilms from cystic fibrosis patients S. aureus was shown to be dominating during childhood, with P. aeruginosa prevalence increasing with aging and worsening patient prognosis 46–48 .…”

Section: Introductionmentioning

confidence: 99%

Bidirectional alterations in antibiotics susceptibility in Staphylococcus aureus - Pseudomonas aeruginosa dual-species biofilm

Kayumov

Trizna

Yarullina

et al. 2018

Preprint

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16While in biofilms bacteria are embedded into an extracellular matrix which forms 17 inaccessible barrier for antimicrobials thereby drastically increasing the concentrations 18 of antibiotics required for treatment. Here we show that the susceptibility of S. aureus 19 and P. aeruginosa to antibiotics in mixed biofilms significantly differs from monoculture 20 biofilms depending on both conditions and chosen antimicrobial agents. While S. aureus 21 could completely avoid vancomycin, ampicillin and ceftriaxone by embedding into the 22 biofilm of P. aeruginosa, the very same consortium was characterized by 10-fold 23 increase in susceptibility to broad-spectrum antimicrobials like ciprofloxacin and 24 aminoglycosides compared to monocultures. These data clearly indicate that efficient 25 treatment of biofilm-associated mixed infections requires antimicrobials active against 26 both pathogens, since the interbacterial antagonism would enhance the efficacy of 27 treatment. Moreover, similar increase in antibiotics efficacy was observed when 28 P. aeruginosa suspension was added to the mature S. aureus biofilm, compared to 29 S. aureus monoculture, and vice versa. These findings open promising perspectives to 30 increase the antimicrobial treatment efficacy of the wounds infected with nosocomial 31 pathogens by the transplantation of the skin residential microflora.32 42 polymicrobial biofilms 11,12 which drastically reduce their susceptibility to both antimicrobials 43 and the immune system of the host 13,14 . Current data suggests that bacterial pathogenicity is 44 promoted during polymicrobial infections and recovery is delayed in comparison with 45 monoculture infections 15-17 . Accordingly, interspecies interactions between S. aureus and 46 P. aeruginosa within mixed biofilms attracted major attention in recent years including both in 47 vitro 15 and in vivo studies 16 . 48 P. aeruginosa is known as a common dominator in polymicrobial biofilm-associated 49 infections due to multiple mechanisms allowing its rapid adaptation to the specific conditions of 50 the host. In particular, P. aeruginosa produces multiple molecules to compete with other 51 microorganisms for space and nutrients. The main anti-staphylococcal tools of P. aeruginosa are 52 siderophores and 2-n-heptyl-4-hydroxyquinoline N-oxide (HQNO), the inhibitor of the electron 53 transport chain of S. aureus. Their presence shifts S. aureus to a fermentative mode of growth, 54 eventually leading to reduced S. aureus viability 18-22 , forces increased S. aureus biofilm 55 formation 23,24 and transition of S. aureus into small-colony variants (SCVs) 25 . SCV is a well-56 characterized phenotype detected in various diseases, including cystic fibrosis and device-related 57 infections 23-26 . SCVs appear as small, smooth colonies on a culture plate and grow significantly 58 slower compared to wild type colonies. Remarkably, switch to the SCV phenotype improves the 59 survival of S. aureus under unfavorable conditions, as it exhibits increased vancomycin and...

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The endotracheal tube microbiome associated with Pseudomonas aeruginosa or Staphylococcus epidermidis

Cited by 50 publications

References 49 publications

In vivo and In vitro Interactions between Pseudomonas aeruginosa and Staphylococcus spp.

In vivo and In vitro Interactions between Pseudomonas aeruginosa and Staphylococcus spp.

Animal models of hospital-acquired pneumonia: current practices and future perspectives

Bidirectional alterations in antibiotics susceptibility in Staphylococcus aureus - Pseudomonas aeruginosa dual-species biofilm

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