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.
Highlights
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
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 shiga toxins (STX)
This study characterizes the response to antibiotic treatment of two isolates, P5711 and P5765, of STEC serotype O104:H4 of the German outbreak in 2011 in comparison to the most common STEC reference strain serotype O157:H7, from the National Reference Centre for Salmonella and other bacterial pathogens causing enteritis, Robert-Koch-Institute, and to the shigatoxinnegative E. coli, ATCC 25922
Summary
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. 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. During the outbreak of a shiga toxin (STX) producing E. coli (STEC), strain O104:H4, in Germany between mid. For the treatment of STEC-infected patients, a causal therapy to prevent the development of HUS is not available. High hopes rest on new therapeutic concepts aiming at binding and inactivating shiga toxin in the patient (for review [2,5]). These approaches are not yet clinically available and applicable
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