Time-resolved @entity3689 uptake of XXXX  erm and concomitant fermentation product and toxin formation.

@entity3534 @entity462 @entity3264 @entity368 @entity1521 @entity344 @entity376 @entity17786 @entity505 @entity72874 @entity3689 @entity413 @entity2718
BACKGROUND: @entity2718 is one of the major nosocomial threats causing severe @entity344 . Compared to the well documented clinical symptoms, little is known about the processes in the bacterial cell like the regulation and activity of metabolic pathways. In this study, we present time-resolved and global data of extracellular substrates and products. In a second part, we focus on the correlation of fermentation products and substrate uptake with toxin production. RESULTS: Formation of different fermentation products during growth in a comparison between the two different media in a global approach was studied using non-targeted gas chromatography-mass spectrometry (GC-MS) based analysis. During cultivation in a @entity72874 medium and minimal medium, the clinical isolate @entity17786  erm showed major differences in @entity3689 utilization: In @entity72874 medium, @entity2718 preferred @entity1521 , @entity368 and @entity462 as @entity505 and energy sources while @entity3264 and @entity376 were not or hardly used. In contrast, @entity1521 and @entity368 were consumed at a significantly later stage in minimal medium. Due to the more complex substrate mixture more fermentation products were detectable in the @entity72874 medium, accompanied by major changes in the ratios between oxidative and reductive Stickland products. Different @entity413 consumption dynamics were observed in presence of either @entity72874 or the minimal set of @entity3534 , accompanied by major changes in butanoate formation. This was associated with a variation in both the toxin yield and a change in the ratio of toxin A to toxin B. CONCLUSIONS: Since in all media compositions, more than one substrate was available as a suitable @entity505 source, availability of different @entity505 sources and their metabolic fate appears to be the key factor for toxin formation.
