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Antimicrobial Agents and Chemotherapy, February 2005, p. 578-583, Vol. 49, No. 2
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.2.578-583.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Tetracycline-Resistant Clinical Helicobacter pylori Isolates with and without Mutations in 16S rRNA-Encoding Genes

Jeng Yih Wu,1,2 Jae J. Kim,3 Rita Reddy,1 W. M. Wang,2 David Y. Graham,1,4 and Dong H. Kwon1*

Veterans Affairs Medical Center and Departments of Medicine,1 Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas,4 Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan,2 Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea3

Received 8 May 2004/ Returned for modification 30 July 2004/ Accepted 4 October 2004

Tetracycline-resistant Helicobacter pylori strains have been increasingly reported worldwide. However, only a small number of tetracycline-resistant strains have been studied with regard to possible mechanisms of resistance and those studies have focused on mutations in the tetracycline binding sites of 16S rRNA-encoding genes. We here report studies of 41 tetracycline-resistant H. pylori strains (tetracycline MICs, 4 to 32 µg/ml) from North America (n = 12) and from East Asia (n = 29). DNA sequence analyses of 16S rRNA-encoding genes revealed that 22 (54%) of the resistant isolates carried one of five different single-nucleotide substitutions (CGA, GGA, TGA, AGC, or AGT) at the putative tetracycline binding site (AGA965-967). Single-nucleotide substitutions were associated with reduced ribosomal binding and with slightly increased tetracycline MICs (1 to 2 µg/ml). The 19 tetracycline-resistant isolates with no detectable mutations in the tetracycline binding site had normal tetracycline-ribosome binding. All tetracycline-resistant isolates, including those with and those without mutations in the tetracycline binding site, showed decreased accumulation of tetracycline. These results suggest that tetracycline resistance is multifactorial, involving alterations both in ribosomal binding and in membrane permeability.

* Corresponding author. Mailing address: Biology Department, Georgia State University, NSC Bldg. 536, University Plaza, Atlanta, GA 30303. Phone: (404) 651-1954. Fax: (404) 651-2509. E-mail: dkwon{at}gsu.edu.

Antimicrobial Agents and Chemotherapy, February 2005, p. 578-583, Vol. 49, No. 2
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.2.578-583.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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