EF, NH, AK, KH, ME and DS carried out the chemical isolations, applications on microbes, and substance identifications. SF carried out the plant culture experiments. MT and SDS conceived and designed the study, RH, NH and HPF participated in its coordination. MT and SDS prepared the manuscript. All authors read and approved the final manuscript.”
“Background During the outbreak of a shiga toxin (STX) producing E. coli (STEC), strain O104:H4, in Germany between mid May and early July 2011, 3842 infected patients were reported of whom 855 developed
a haemolytic-uremic syndrome (HUS) Selleckchem KU55933 and 53 died [1]. In the light of outbreaks of STEC transmitted by contaminated food at unpredictable Regorafenib molecular weight intervals all over the world, these recent numbers underline the serious threat posed by STEC to public
health even in highly developed countries. For the treatment of STEC-infected patients, a causal therapy to prevent the development of HUS is not available. Most importantly, the use of antibiotics is controversially discussed due to the particular response of STEC. According to the prevailing view, the use of antibiotics against STEC should be avoided because it is assumed to increase the risk of developing HUS (for review[2]). Although SGLT inhibitor growth of given STEC strains is susceptible to inhibition by specific antibiotics, the bacteria may respond with enhanced release of shiga toxin activity [3, 4]. High hopes rest on new therapeutic concepts aiming at binding and inactivating shiga toxin in the patient (for review [2, 5]). However, these approaches are not yet
clinically available and applicable. L-NAME HCl The recent STEC outbreak prompted us to revisit the effects of antibiotics on STEC. These effects have been studied intensively in the most common STEC serotype O157:H7 that emerged as a human pathogen in 1982 [6]. Treatment of this STEC strain with antibiotics, specifically with those interfering with DNA replication, activates the SOS response of the bacteria [7]. This in turn activates the lytic cycle of the bacteriophages that encode, among others, the shigatoxin genes. Consequences are, first, the increased production of STX and, second, phage-induced lysis of E. coli host cells eventually resulting in the release of large amounts of STX. The influence of antibiotic treatment upon the clinical course including the frequency of HUS within the cohort of STEC-infected patients had been assessed mostly in retrospective studies [8, 9]. So far, neither observations during outbreaks nor controlled clinical trials provided resilient evidence whether early and consequent antibiotic treatment of STEC-infected individuals might be effective to reliably abort the release of STX thereby preventing the development or aggravation of HUS. Notably, clinical observations as well as most studies in vitro focussed on O157:H7, being the most frequent serotype of STEC.
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