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Antimicrobial Agents and Chemotherapy, June 2005, p. 2302-2306, Vol. 49, No. 6
0066-4804/05/$08.00+0 doi:10.1128/AAC.49.6.2302-2306.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Laboratory of Infectious Agents Surveillance, Kitasato Institute for Life Sciences, Kitasato University, 5-9-1 Shirokane, Minatoku, Tokyo, Japan,1 Kitasato Institute for Life Sciences & Graduate School of Infection Control Sciences, Kitasato University, Tokyo, Japan,2 National Hospital Organization Tokyo Medical Center, Tokyo, Japan,3 Medical Corporation Nagatsu-kai Saito Hospital, Chiba, Japan,4 Osaka Rosai Hospital, Osaka, Japan,5 Hakujikai Memorial Hospital, Tokyo, Japan,6 Saiseikai Ibaraki Hospital, Osaka, Japan7
Received 7 October 2004/ Returned for modification 5 December 2004/ Accepted 31 January 2005
A total of 195 Mycoplasma pneumoniae strains were isolated from 2,462 clinical specimens collected between April 2002 and March 2004 from pediatric outpatients with respiratory tract infections. Susceptibilities to six macrolide antibiotics (ML), telithromycin, minocycline, levofloxacin, and sitafloxacin were determined by the microdilution method using PPLO broth. A total of 183 M. pneumoniae isolates were susceptible to all agents and had excellent MIC90s in the following order: 0.00195 µg/ml for azithromycin and telithromycin, 0.0078 µg/ml for clarithromycin, 0.0156 µg/ml for erythromycin, 0.0625 µg/ml for sitafloxacin, 0.5 µg/ml for minocycline, and 1 µg/ml for levofloxacin. Notably, 12 ML-resistant M. pneumoniae strains were isolated from patients with pneumonia (10 strains) or acute bronchitis (2 strains). These strains showed resistance to ML with MICs of
1 µg/ml, except to rokitamycin. Transition mutations of A2063G or A2064G, which correspond to A2058 and A2059 in Escherichia coli, in domain V on the 23S rRNA gene in 11 ML-resistant strains were identified. By pulsed-field gel electrophoresis typing, these strains were classified into groups I and Vb, as described previously (A. Cousin-Allery, A. Charron, B. D. Barbeyrac, G. Fremy, J. S. Jensen, H. Renaudin, and C. Bebear, Epidemiol. Infect. 124:103-111, 2000). These findings suggest that excessive usage of MLs acts as a trigger to select mutations on the corresponding 23S rRNA gene with the resultant occurrence of ML-resistant M. pneumoniae. Monitoring ML susceptibilities for M. pneumoniae is necessary in the future.
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