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Background: The shiga toxin-producing E. coli (STEC) O104:H4 caused a major outbreak in Germany in spring 2011. STEC are usually susceptible to common antibiotics. However, antibiotic treatment of STEC-infected patients is not recommended because STEC may enhance production and release of shiga toxins (STX) in response to antibiotics, which eventually enhances the frequency and severity of clinical symptoms, including haemolytic uraemic syndrome (HUS) and fatalities., Results: We characterized the response to antibiotics of STEC O104:H4 isolates from two HUS patients during the German STEC outbreak in spring 2011 in comparison to the common STEC O157:H7. Liquid cultures of STEC O157:H7 and O104:H4 were incubated with graded dilutions of the antibiotics ciprofloxacin, meropenem, fosfomycin, gentamicin, rifampicin, and chloramphenicol. At defined times of antibiotic treatment, transcriptional activation of the STX2 gene, contents of STX and STX-activity in the culture supernatants were quantified. Unlike the common serotype O157:H7, STEC O104:H4 does not release STX in response to therapeutic concentrations of ciprofloxacin, meropenem, fosfomycin, and chloramphenicol., Conclusions: In future outbreaks, the response of the respective epidemiologic STEC strain to antibiotics should be rapidly characterized in order to identify antibiotics that do not enhance the release of STX. This will eventually allow clinical studies tackling the question whether antibiotic treatment impacts on the eradication of STEC, clinical course of disease, and frequency of carriers.

A method for the simultaneous determination of polar pharmaceutical compounds in water is presented. Samples from 27 rivers and ponds were investigated for contents of Gemfibrocil, a lipid blood regulating compound, Clofibric acid, a metabolite of lipid regulating compounds (Clofibrat, Etofibrat, Etofyllinclofibrat), antirheumatics (Diclofenac, Ibuprofen, Ketoprofen, Indomethacin, Fenoprofen) and Sarkosin-N-(phenylsulfonyl) (SPS), a metabolite of a corrosion inhibiting agent. In addition water samples were investigated for some main metabolites of Ibuprofen, 2-[4-(2-hydroxy-2-methylpropyl)phenyl]propionic acid (hydroxy-ibuprofen) and 2-[4-(2-carboxypropyl)phenyl]propionic acid (carboxy-ibuprofen), which are excreted after oral intake. For gas chromatographic analysis the drugs were converted into their methyl-derivatives by "on column" reaction with TMSH, TMAH and "pre column" with diazomethane. The detection limits with TMSH were in the same range or lower than those with diazomethane or TMAH. The compound most frequently found was SPS which was only absent in waters with natural surroundings. Diclofenac could be detected in 10 out of 27 water samples in concentrations of up to 15 micrograms/l. In contrast, none of the pharmaceuticals investigated were present in 8 drinking water samples from Cologne and surroundings. Though concentrations measured were far below pharmacological doses, the data suggest a steady flux of these drugs into the environment.