title: [In vitro antibacterial activity of faropenem, a novel oral penem antibiotic, against enterohemorrhagic Escherichia coli O157 strains].
abstract: Against enterohemorrhagic Escherichia coli (EHEC) O157 clinically isolated, the effects of faropenem (FRPM), a novel oral penem antibiotic, on the MICs, bactericidal activity, verotoxin (VT)-release, and lipopolysaccharide (LPS)-release were investigated in vitro and compared with those of other types of antibacterial agents. The MICs of FRPM in aerobic and anaerobic culture condition, were 0.78 and 0.39 microgram/ml, respectively. In aerobic condition, FRPM was more active than ampicillin, amoxicillin (AMPC), fosfomycin (FOM), kanamycin (KM), minocycline (MINO), and clarithromycin (CAM), but was slightly less active than cefdinir (CFDN), cefditoren (CDTR), and norfloxacin (NFLX) against O157 clinical isolates. In anaerobic condition, however, FRPM showed as strong activity as CFDN, CDTR, and NFLX. FOM, NFLX, and KM as well as the beta-lactams including FRPM indicated the powerful bactericidal activity against one strain of O157 clinical isolates. The effects of MINO and CAM were bacteriostatic. FOM and the beta-lactams including FRPM promoted verotoxin type 1 (VT1)-release, but rather suppressed verotoxin type 2 (VT2)-release from the same isolate. NFLX, however, promoted VT1-release and vast amount of VT2-release. In the case of KM, MINO, and CAM, the release suppression of both VT1 and VT2 was observed. FRPM, AMPC, and FOM had very weak activity on LPS-release, while CFDN, CDTR, and NFLX released a large amount of LPS from the strain. KM, MINO, and CAM had relatively weak activity. In these in vitro experiments, FRPM demonstrated the effective profile to the treatment for EHEC infection, except for the effect on VT1-release. These results suggest the possibility that FRPM shows good clinical efficacy for EHEC infection.
authors.affiliation: Suntory Institute for Biomedical Research.
authors.forename: T
authors.initials: T
authors.lastname: Nasu
authors.forename: K
authors.initials: K
authors.lastname: Okamoto
authors.forename: T
authors.initials: T
authors.lastname: Nakanishi
authors.forename: T
authors.initials: T
authors.lastname: Nishino
mesh_terms: D000658:Amoxicillin / Q000494:pharmacology; D000667:Ampicillin / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001427:Bacterial Toxins / Q000378:metabolism; D000077525:Cefdinir; D002511:Cephalosporins / Q000494:pharmacology; D017291:Clarithromycin / Q000494:pharmacology; D019453:Escherichia coli O157 / Q000187:drug effects* / Q000378:metabolism; D005578:Fosfomycin / Q000494:pharmacology; D007612:Kanamycin / Q000494:pharmacology; D007769:Lactams; D008826:Microbial Sensitivity Tests; D008911:Minocycline / Q000494:pharmacology; D009643:Norfloxacin / Q000494:pharmacology; D022622:Shiga Toxin 1; D047090:beta-Lactams
chemical_list: D000900:Anti-Bacterial Agents; D001427:Bacterial Toxins; D002511:Cephalosporins; D007769:Lactams; D022622:Shiga Toxin 1; D047090:beta-Lactams; D005578:Fosfomycin; D007612:Kanamycin; D000667:Ampicillin; D000658:Amoxicillin; C073460:cefditoren; D000077525:Cefdinir; C107057:fropenem; D008911:Minocycline; D017291:Clarithromycin; D009643:Norfloxacin