In Selleck RG7112 contrast, fosfomycin did not significantly alter at any concentration the STX activity in supernatants of STEC O104:H4 cultures. Gentamicin did not affect the STX activity in the supernatants of STEC strains O157:H7 or O104:H4 at any concentration

(Figure 3D). Rifampicin at 0.25x to 4x MIC increased the STX activity in the supernatants of both STEC O157:H7 and O104:H4 up to 10-fold (Figure 3E). Chloramphenicol at 1x and 4x MIC reduced the STX activity in supernatants of both strains O157:H7 and O104:H4 up to 10-fold (Figure 3F). Taken together, the titers of STX as determined by EIA and the STX activity as measured by Vero cell cytotoxicity assay are concordant. SCH727965 They show that meropenem and fosfomycin at any concentration do not induce the release of STX from STEC O104:H4 and that the 4x MIC of both antibiotics even decreases the STX activity in comparison to untreated controls. Collectively, our data demonstrate that the effect of a given antibiotic upon the release of STX from a newly emerging STEC strain must not be deduced from the effect on O157:H7 or any other non-related STEC strain. Specifically, ciprofloxacin, meropenem and fosfomycin

should be considered for the treatment of infections caused by strain O104:H4. Discussion STEC strain O104:H4 caused the large outbreak of STEC in spring 2011 in Germany. Antibiotic treatment of STEC infected patients is generally not recommended, because enhanced release of STX from

STEC O157:H7 has been reported associated with the fear of enhancing the frequency of HUS and fatalities (reviewed in [2]). This report characterizes the response of the selleck screening library German outbreak STEC strain O104:H4 in comparison to the prototypic STEC O157:H7. The results of this study should help to illuminate present and future medical practice. The mechanisms of the antibiotic-induced production and release of STX by STEC have extensively been characterized in vitro for the most frequent STEC strain, O157:H7. Our study confirms previous reports showing enhanced STX production and release by O157:H7 in the presence of diverse antibiotics. In stark contrast, the German outbreak STEC strain O104:H4 responded to several antibiotics differently with either no release of STX or even reduced STX-titers. These data further confirm and extend previous reports that the release of STX by STEC in response selleck products to antibiotics is highly dependent on the strain of STEC and the concentration of the antibiotic [3, 4]. For this study, two randomly picked different isolates, P5711 and P5765, of E. coli O104:H4 were used that were isolated from two independent patients at the Medical Center of Cologne University during the German outbreak of STEC O104:H4 in spring 2011. It should be noted that these isolates responded highly concordant to antibiotic treatment as it should be expected due to the assumed clonal origin of pathogenic microorganisms during a defined outbreak.