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Matthias Willmann

Researcher at University of Tübingen

Publications -  46
Citations -  1810

Matthias Willmann is an academic researcher from University of Tübingen. The author has contributed to research in topics: Pseudomonas aeruginosa & Drug resistance. The author has an hindex of 18, co-authored 45 publications receiving 1344 citations. Previous affiliations of Matthias Willmann include Max Planck Society.

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Human commensals producing a novel antibiotic impair pathogen colonization

TL;DR: It is shown that nasal Staphylococcus lugdunensis strains produce lugdunin, a novel thiazolidine-containing cyclic peptide antibiotic that prohibits colonization by S. aureus, and a rare example of a non-ribosomally synthesized bioactive compound from human-associated bacteria.
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Evaluation of the Accelerate Pheno System for Fast Identification and Antimicrobial Susceptibility Testing from Positive Blood Cultures in Bloodstream Infections Caused by Gram-Negative Pathogens.

TL;DR: The Accelerate Pheno system provided fast, reliable results while significantly improving turnaround time in blood culture diagnostics of Gram-negative BSI and compared to conventional culture-based methods in the laboratory setting.
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Distinct impact of antibiotics on the gut microbiome and resistome: a longitudinal multicenter cohort study

TL;DR: This study quantified changes in the gut microbiome in two cohorts of hematological patients receiving prophylactic antibiotics and found that factors such as individual baseline microbiome, resistome, and plasmid diversity; liver/kidney function; and concurrent medication, especially virostatic agents, influence resistome alterations.
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Prevalence and risk factors associated with colonization and infection of extensively drug-resistant Pseudomonas aeruginosa: a systematic review.

TL;DR: Risk factors independently associated with XDR P. aeruginosa colonization or infections are described in four groups with reference to antimicrobial therapy, medical devices as well as patient- and hospital environment-related factors.