MB has performed in part the cell culture experiments. AF has acquisitioned, analyzed and interpreted the chromatographic data. CA did the statistical analysis. HW has designed and constructed the system for bacteria cultivation

and collection of headspace samples. MN, JT and AA have designed the study, discussed the results and finalized the manuscript. All authors read and approved the final manuscript.”
“Background Shiga toxin-producing Escherichia coli (STEC) are members of a category of pathogenic E. coli that see more can cause illness ranging from mild intestinal diarrheal disease to severe kidney complications, such as hemolytic uremic syndrome (HUS; reviewed in [1]). Cases and outbreaks of STEC have been associated with the consumption of contaminated food and water. Although more than 100 serogroups have been implicated, the major outbreaks are linked to a very small selleck number of serotypes (reviewed in [2]). In 2011, an uncommon strain of pathogenic E. coli serotype O104:H4 caused an unusual number of gastroenteritis and HUS cases, occurring

predominantly in adults. The strain originated in northern Germany and disseminated to other European countries [3–5]. The outbreak was originally thought to have been caused by a STEC strain, but was later shown to be produced as a result of an enteroaggregative E. coli (EAEC) strain that had acquired the genes for production of Shiga toxins [6–9]. The EAEC category is heterogeneous, and it is associated with cases of acute Megestrol Acetate or persistent diarrhea in children and adults worldwide (reviewed in [10, 11]). The virulence of EAEC is known to require a variety of virulence factors. The mechanism by which EAEC exerts pathogenesis; however, is thus far poorly check details characterized since EAEC strains are recovered from healthy as well as diseased subjects (reviewed in [10, 11]). EAEC strains are recognized by their characteristic aggregative or “”stacked-brick”" adherence pattern and their ability to form biofilms. It has been proposed that host cellular changes during EAEC infection results in digestive-absorptive

abnormalities, prolonging the diarrhea [12]. The ability of EAEC to obtain essential nutrients during this process and multiply successfully in this environment is crucial. EAEC, like most bacteria, must acquire iron to survive, since the inability to acquire this metal will disrupt biofilm formation properties and EAEC interaction with human epithelial cells [13]. Therefore, EAEC strains attempting to establish an infection must have the ability to scavenge iron and multiply within the host environment as fundamental requirements for the disease onset. A wide variety of strategies for acquiring iron have been developed by pathogenic E. coli, the most common being the production of siderophores and the utilization of heme [14]. Okeke et al.