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Antimicrobial Agents and Chemotherapy, December 2004, p. 4624-4630, Vol. 48, No. 12
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.12.4624-4630.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Characterization and Molecular Analysis of Macrolide-Resistant Mycoplasma pneumoniae Clinical Isolates Obtained in Japan

Mayumi Matsuoka,1 Mitsuo Narita,2 Norio Okazaki,3 Hitomi Ohya,3 Tsutomu Yamazaki,4 Kazunobu Ouchi,5 Isao Suzuki,6 Tomoaki Andoh,6 Tsuyoshi Kenri,1 Yuko Sasaki,1 Atsuko Horino,1 Miharu Shintani,1 Yoshichika Arakawa,1 and Tsuguo Sasaki1*

Department of Bacterial Pathogenesis and Infection Control, National Institute of Infectious Diseases, Tokyo,1 Sapporo Tetsudo Hospital, Hokkaido,2 Kanagawa Prefectural Institute of Public Health,3 Department of Pediatrics, Chigasaki Municipal Hospital, Kanagawa,6 Department of Infection Control, Saitama Medical School, Saitama,4 Department of Pediatrics II, Kawasaki Medical School, Okayama, Japan5

Received 28 April 2004/ Returned for modification 11 July 2004/ Accepted 1 August 2004

In recent years, Mycoplasma pneumoniae strains that are clinically resistant to macrolide antibiotics have occasionally been encountered in Japan. Of 76 strains of M. pneumoniae isolated in three different areas in Japan during 2000 to 2003, 13 strains were erythromycin (ERY) resistant. Of these 13 strains, 12 were highly ERY resistant (MIC, ≥256 µg/ml) and 1 was weakly resistant (MIC, 8 µg/ml). Nucleotide sequencing of domains II and V of 23S rRNA and ribosomal proteins L4 and L22, which are associated with ERY resistance, showed that 10 strains had an A-to-G transition at position 2063 (corresponding to 2058 in Escherichia coli numbering), 1 strain showed A-to-C transversion at position 2063, 1 strain showed an A-to-G transition at position 2064, and the weakly ERY-resistant strain showed C-to-G transversion at position 2617 (corresponding to 2611 in E. coli numbering) of domain V. Domain II and ribosomal proteins L4 and L22 were not involved in the ERY resistance of these clinical M. pneumoniae strains. In addition, by using our established restriction fragment length polymorphism technique to detect point mutations of PCR products for domain V of the 23S rRNA gene of M. pneumoniae, we found that 23 (24%) of 94 PCR-positive oral samples taken from children with respiratory infections showed A2063G mutation. These results suggest that ERY-resistant M. pneumoniae infection is not unusual in Japan.

* Corresponding author. Mailing address: Department of Bacterial Pathogenesis and Infection Control, National Institute of Infectious Diseases, 4-7-1 Gakuen, Musashimurayama-shi, Tokyo 208-0011, Japan. Phone: (81) 425610771. Fax: (81) 425653315. E-mail: sasaki{at}nih.go.jp.

Antimicrobial Agents and Chemotherapy, December 2004, p. 4624-4630, Vol. 48, No. 12
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.12.4624-4630.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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