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Antimicrobial Agents and Chemotherapy, December 2003, p. 3719-3723, Vol. 47, No. 12
0066-4804/03/$08.00+0 DOI: 10.1128/AAC.47.12.3719-3723.2003
Copyright © 2003, American
Society for
Microbiology. All Rights Reserved.
Department of Microbiology, Kyungpook National University School of Medicine, Taegu 700-422,1 Department of Microbiology, Eulji University School of Medicine, Taejeon 301-832,Korea2
Received 8 May 2003/ Returned for modification 3 July 2003/ Accepted 19 August 2003
The
resistance to ampicillin and nalidixic acid in Shigella sonnei
isolates obtained in Korea during the period 1998 to 2000 was
characterized. Recently (J. Y. Oh, H. S. Yu,
S. K. Kim, S. Y. Seol, D. T. Cho, and
J. C. Lee, J. Clin. Microbiol. 41:421-423,
2003) ampicillin and nalidixic acid resistance was found in 49 and
70%, respectively, of the 67 S. sonnei isolates
obtained during this period. We analyzed 138 S. sonnei
isolates collected during the same period. Ampicillin and nalidixic
acid resistance was found in 30 and 86% of the isolates,
respectively. The ampicillin resistance was mediated by a TEM-1
ß-lactamase, and TEM-52 extended-spectrum ß-lactamase
was identified in one sporadic S. sonnei isolate from 1999.
blaTEM-1 and blaTEM-52 were
located in conjugative R-plasmids. Tn3 was detected in
41% of the ampicillin-resistant isolates. The R-plasmids from
the transconjugants that transferred resistance to ampicillin exhibited
different restriction fragment length polymorphism patterns, and a
blaTEM-1 probe was hybridized with the different
fragments. The nalidixic acid resistance was exclusively associated
with an amino acid substitution, Ser83
Leu (TCG
TTG),
in gyrA. These findings indicate that the genetically related
S. sonnei strains readily acquire resistance to ampicillin,
streptomycin, trimethoprim, and sulfamethoxazole but not nalidixic acid
through conjugative R-plasmids from difference sources when confronted
by antibiotic selective
pressures.
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