Evidence map›Paper›PMID 27734161›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2017

Determinants for persistence of Pseudomonas aeruginosa in hospitals: interplay between resistance, virulence and biofilm formation.

S J Kaiser, N T Mutters, A DeRosa, C Ewers, U Frank, F Günther

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Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Adaptive evolution ofMicrobial genomics · 2026
    Article
  5. Article
  6. Modern antiseptics against multidrug-resistantFrontiers in microbiology · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Distribution of carbapenem resistance mechanisms in clinical isolates of XDR Pseudomonas aeruginosa.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

S J KaiserDepartment of Infectious Diseases, Heidelberg University Hospital, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany.
N T MuttersDepartment of Infectious Diseases, Heidelberg University Hospital, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany.
A DeRosaDepartment of Infectious Diseases, Sapienza University of Rome, Rome, Italy.
C EwersInstitute of Hygiene and Infectious Diseases of Animals, Justus Liebig University Giessen, Giessen, Germany.
U FrankDepartment of Infectious Diseases, Heidelberg University Hospital, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany.
F GüntherDepartment of Infectious Diseases, Heidelberg University Hospital, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany. frank.guenther@med.uni-heidelberg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa (Pa) is one of the major bacterial pathogens causing nosocomial infections. During the past few decades, multidrug-resistant (MDR) and extensively drug-resistant (XDR) lineages of Pa have emerged in hospital settings with increasing numbers. However, it remains unclear which determinants of Pa facilitated this spread. A total of 211 clinical XDR and 38 susceptible clinical Pa isolates (nonXDR), as well as 47 environmental isolates (EI), were collected at the Heidelberg University Hospital. We used RAPD PCR to identify genetic clusters. Carriage of carbapenamases (CPM) and virulence genes were analyzed by PCR, biofilm formation capacity was assessed, in vitro fitness was evaluated using competitive growth assays, and interaction with the host's immune system was analyzed using serum killing and neutrophil killing assays. XDR isolates showed significantly elevated biofilm formation (p < 0.05) and higher competitive fitness compared to nonXDR and EI isolates. Thirty percent (62/205) of the XDR isolates carried a CPM. Similarities in distribution of virulence factors, as well as biofilm formation properties, between CPM+ Pa isolates and EI and between CPM- and nonXDR isolates were detected. Molecular typing revealed two distinct genetic clusters within the XDR population, which were characterized by even higher biofilm formation. In contrast, XDR isolates were more susceptible to the immune response than nonXDR isolates. Our study provides evidence that the ability to form biofilms is an outstanding determinant for persistence and endemic spread of Pa in the hospital setting.

Indexed as

HospitalsBacterial Proteinsbeta-LactamasesBiofilmsCluster AnalysisCross InfectionDrug Resistance, Multiple, BacterialEnvironmental MicrobiologyGenotypeHumansMolecular TypingPolymerase Chain ReactionPseudomonas aeruginosaPseudomonas InfectionsRandom Amplified Polymorphic DNA TechniqueVirulenceBacterial Proteinsbeta-LactamasescarbapenemaseVirulence Factors

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.