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Gene and cytokine profile analysis of macrolide-resistant Mycoplasma pneumoniae infection in Fukuoka, Japan

Kentaro Matsuda12*, Mitsuo Narita3, Nobuyuki Sera4, Eriko Maeda4, Hideaki Yoshitomi4, Hitomi Ohya5, Yuko Araki6, Tatsuyuki Kakuma6, Atsushi Fukuoh7 and Kenji Matsumoto2

Author Affiliations

1 Matsuda Children’s Clinic, Fukuoka, Japan

2 Department of Allergy and Immunology, National Research Institute for Child Health and Development, Setagaya, Tokyo, Japan

3 Department of Pediatrics, Sapporo Tokushukai Hospital, Sapporo, Hokkaido, Japan

4 Division of Virology, Fukuoka Institute of Health and Environmental Sciences, Dazaifu, Fukuoka, Japan

5 Division of Microbilogy, Kanagawa Prefectural Institute of Public Health, Chigasaki, Kanagawa, Japan

6 Biostatics Center, Kurume University School of Medicine, Kurume, Fukuoka, Japan

7 Department of Medical Laboratory Science, Junshin Gakuen University, Fukuoka, Fukuoka, Japan

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BMC Infectious Diseases 2013, 13:591  doi:10.1186/1471-2334-13-591

Published: 16 December 2013



Recent epidemiologic data suggest that the prevalence of macrolide resistant Mycoplasma pneumoniae (MR-M. pneumoniae) is increasing rapidly worldwide. This study assessed the present status of M. pneumoniae infection in Japan and clinical end-points to distinguish children with MR-M. pneumoniae.


During an outbreak of M. pneumoniae infections in Fukuoka, Japan in 2010–11, a total of 105 children with clinically suspected M. pneumoniae infection were enrolled. M. pneumoniae was analyzed for macrolide resistance in domain V of the 23S rRNA gene. Sixty -five patients with PCR positive for M. pneumoniae were analyzed with regard to clinical symptoms, efficacy of several antimicrobial agents and several laboratory data.


Causative pathogens were detected in 81.0% (85 of 105) and M. pneumoniae was identified 61.9% (65 of 105). The resistance rate of M. pneumoniae was 89.2% (58 of 65) in this general pediatric outpatient setting. Patients infected with MR-M. pneumoniae showed longer times to resolution of fever and required frequent changes of the initially prescribed macrolide to another antimicrobial agent. We observed three different genotypes of M. pneumoniae including the rarely reported A2063T mutation (A2063G: 31 strains, A2063T: 27 strains, no mutation: 7 strains). Drug susceptibility testing showed different antimicrobial susceptibility profiles for each genotype. Serum IFN-gamma, IL-6 and IP-10 levels were higher in patients with MR-genotypes than in those infected with no-mutation strains (p < 0.001).


Macrolide resistance is more common than previously thought and a small epidemic of rarely reported A2063T mutation was observed in Fukuoka, Japan. Furthermore our results reveal the possibility that levels of certain inflammatory cytokines may be a candidate to predict MR-M.pneumoniae infection.

Mycoplasma pneumoniae; Macrolide resistant; A2063T; Inflammatory cytokine; Predictive factors