report about the central Scotland outbreak of STEC O157:H7 in 1996 [8]. These authors state that selleckchem coincidental treatment of STEC-infected patients with antibiotics for other diseases is a risk factor for HUS and fatalities. However, such a coincidental, non-targeted antibiotic treatment cannot replace a validated, high-dose treatment specifically targeted against a defined STEC strain. Similarly, in a Japanese outbreak of STEC O157:H7 among school children, fosfomycin was used as the “most commonly prescribed antimicrobial agent in Japan” but not because it was validated as effective and safe in the treatment of this STEC strain [9]. Other clinical studies [16–18] as well as a metaanalysis [15] did

not reveal a correlation between

the use of antibiotics and the frequencies of the development of HUS. Consequently, in medical practice antibiotic treatment of patients infected with STEC is avoided. However, it seems unjustified to forfeit generally the antibiotic eradication of STEC and resort only to symptomatic treatment of BIBF 1120 mw STEC patients. Animal studies have revealed that treatment with various antibiotics on days 1 to 3 after infection with STEC O157:H7 reduced in mice the STX levels in the blood and stool, shortened the duration of excretion of the bacteria, and all antibiotic-treated mice survived the otherwise lethal infection [19]. Similarly, mice infected with STEC O157:H7 showed enhanced survival after treatment with rifampicin alone [20] or after a sequential therapy with low dose rifampicin followed by high dose gentamicin [21]. During the final preparation of this report, Karch´s group published similar data of their concurrent study of the effects of subinhibitory concentrations of antibiotics on the German outbreak strain STEC O104:H4 with regard to the induction and release of STX [22]. In both studies, almost identical tetracosactide responses of STEC O104:H4 to the antibiotics meropenem,

fosfomycin, gentamicin, rifampicin, and chloramphenicol were observed. At the first glance, the responses of both the outbreak strain O104:H4 and the reference strain O157:H7 seemingly differs somewhat between both reports. However, these differences are apparently due to differences in the experimental conditions applied by each group. Among these are (i) different bacterial densities at the start of antibiotic treatment (OD600 of 0.5 in Bielaszewska´s study versus 1×108 cells/ml (corresponding to an OD600 of 0.1 in our hands)), (ii) analysis of induction of STX2-transcripts after 15 h versus 2 h of antibiotic treatment, (iii) or incubating Vero cells in cytotoxicity assays for 72 h versus 48 h with STX2-containing supernatants. Altogether, both reports with slightly different concepts and approaches confirm each other and therefore clearly show the potential for future controlled clinical studies using antibiotic treatment of patients infected with specific STEC strains.

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