ArticleBMC microbiology2012
Therapeutic concentrations of antibiotics inhibit Shiga toxin release from enterohemorrhagic E. coli O104:H4 from the 2011 German outbreak.
Article in BMC microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 72 citations in OpenAlex.
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- Shiga Toxin-Producing E. coli and Hemolytic Uremic Syndrome: A Study of the 2022 Outbreak in Turkey.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Do asymptomatic STEC-long-term carriers need to be isolated or decolonized? New evidence from a community case study and concepts in favor of an individualized strategy.Frontiers in public health · 2024Article
- Prevalence, virulence factors, and antimicrobial resistance profiles of Shiga toxin-producingVeterinary research forum : an international quarterly journal · 2023Article
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- An in vitro fermentation model to study the impact of bacteriophages targeting Shiga toxin-encoding Escherichia coli on the colonic microbiota.NPJ biofilms and microbiomes · 2022Article
- EnterohemorrhagicInternational journal of molecular sciences · 2022Review
- Prevalence of genotypic antimicrobial resistance in clinical Shiga toxin-producingJournal of medical microbiology · 2021Article
- Article
- Insights into Emergence of Antibiotic Resistance in Acid-Adapted EnterohaemorrhagicAntibiotics (Basel, Switzerland) · 2021Review
- Issues beyond resistance: inadequate antibiotic therapy and bacterial hypervirulence.FEMS microbes · 2020Review
- Potentiation of Antibiotics by a Novel Antimicrobial Peptide against Shiga Toxin Producing E. coli O157:H7.Scientific reports · 2020Article
- Glomerulonephritis in AKI: From Pathogenesis to Therapeutic Intervention.Frontiers in medicine · 2020Review
- Treatment Strategies for Infections With Shiga Toxin-ProducingFrontiers in cellular and infection microbiology · 2020Review
- Transcriptional and Translational Inhibitors Block SOS Response and Shiga Toxin Expression in Enterohemorrhagic Escherichia coli.Scientific reports · 2019Article
- O-serogroups, virulence genes, antimicrobial susceptibility, and MLST genotypes of Shiga toxin-producing Escherichia coli from swine and cattle in Central China.BMC veterinary research · 2019Article
- Hemolytic uremic syndrome in a developing country: Consensus guidelines.Pediatric nephrology (Berlin, Germany) · 2019Article
- A pediatric neurologic assessment score may drive the eculizumab-based treatment of Escherichia coli-related hemolytic uremic syndrome with neurological involvement.Pediatric nephrology (Berlin, Germany) · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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