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Antimicrobial Agents and Chemotherapy, April 1999, p. 789-793, Vol. 43, No. 4
Department of Bacteriology, Nagoya University
School of Medicine, Showa-ku, Nagoya 466-8550, Japan
Received 10 August 1998/Returned for modification 24 November
1998/Accepted 24 January 1999
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 (
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Copyright © 1999, American Society for Microbiology. All rights reserved.
Emergence of Fosfomycin-Resistant Isolates of
Shiga-Like Toxin-Producing Escherichia coli O26
128 µg/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 µg/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-
-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.
*
Corresponding author. Mailing address: Department of
Bacteriology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Phone: 81-52-744-2101. Fax: 81-52-744-2107. E-mail:
horii{at}tsuru.med.nagoya-u.ac.jp.
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