Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Horii, T. et al.

Horii, Kimura, Sato, Shibayama, Ohta,

Emergence of fosfomycin-resistant isolates of Shiga-like toxin-producing Escherichia coli O26.

We evaluated the susceptibilities of 129 Shiga-like toxin-producing Escherichia coli (STEC) isolates to various antibiotics. The numbers of isolates for which MICs were high (> or = 128 micrograms/ml) were as follows: 5 for fosfomycin, 14 for ampicillin, 1 for cefaclor, 6 for kanamycin, 22 for tetracycline, and 2 for doxycycline. For two isolates of STEC O26 MICs of fosfomycin were high (1,024 and 512 micrograms/ml, respectively). Conjugation experiments and glutathione S-transferase assays suggested that the fosfomycin resistance in these isolates was determined not by a plasmid but chromosomally. The amount of active intracellular fosfomycin in these STEC isolates was 100- to 200-fold less than that in E. coli C600 harboring pREFTT47B408 in the presence of either L-alpha-glycerophosphate or glucose-6-phosphate. Cloning, sequencing, and Northern blot analysis demonstrated that the transcriptional level of the murA gene encoding UDP-N-acetylglucosamine enolpyruvoyl transferase in these isolates was greater than that in E. coli C600. Our results suggest that the fosfomycin resistance in these STEC isolates is due to concurrent effects of alteration of the glpT and/or uhp transport systems and of the enhanced transcription of the murA gene.[1]

References

Emergence of fosfomycin-resistant isolates of Shiga-like toxin-producing Escherichia coli O26. Horii, T., Kimura, T., Sato, K., Shibayama, K., Ohta, M. Antimicrob. Agents Chemother. (1999) [Pubmed]

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