Therapeutic concentrations of antibiotics inhibit Shiga toxin release from enterohemorrhagic E. coli O104:H4 from the 2011 German outbreak

Abstract

BackgroundThe 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.ResultsWe 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.ConclusionsIn 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.

Effect of Rifampicin and Gentamicin on Shiga Toxin 2 Expression Level and the SOS Response inEscherichia coliO104:H4

“…Moreover, the study showed a similar effect of rifampicin at the sub-MIC level on the stx2 transcription levels and Stx2 release. In addition, it indicated similar results when compared to our study when E. coli O104:H4 was subjected to the MIC and the sub-MIC of gentamicin (Corogeanu et al, 2012). Similar results with gentamicin at the sub-MIC level in one strain of E. coli O104:H4 were observed in another study done by Bielaszewska et al; however, these results were insignificant (Bielaszewska et al, 2012).…”

Phenethyl Isothiocyanate Inhibits Shiga Toxin Production in Enterohemorrhagic Escherichia coli by Stringent Response Induction

“…The effects of some antibiotics were strongly dependent on their concentrations, causing either an increase or decrease in efficiency of Shiga toxin production (44)(45)(46). In this light, it is important to note that it was reported recently that STEC strain O104:H4, which caused a recent outbreak in Germany, did not release Shiga toxin in response to therapeutic concentrations of ciprofloxacin, meropenem, fosfomycin, and chloramphenicol (47). Definitely, different classes of antibiotics differentially influence Shiga toxin production (48), and effects of particular antibiotics are dependent on their concentrations.…”

Hemolytic uremic syndrome associated withAcinetobacter hemolyticus

“…[15][16][17] However, recent reports during a German outbreak established new evidence regarding antibiotic usage. [18][19][20] In conclusion, Acinetobacter infection should be considered as a plausible cause of typical HUS in cases with no E. coli infection. The high frequency and degree of adaptability and transformability among some strains of Acinetobacter spp.…”