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A3592 - First Adult Case of Fulminant Mycoplasma Pneumoniae Pneumonia Due to a Macrolide-Resistant Strain Successfully Treated with Quinolone and Minocycline
Author Block: M. Matsumoto1, K. Nagaoka1, M. Suzuki2, Y. Yamashita1, N. Takei2, H. Kimura2, S. Konno3, N. Ishiguro4, M. Nishimura5; 1Department of Respiratory Medicine, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan, 2First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan, 3Hokkaido Univ, School of Med, Sapporo, Japan, 4Department of Infection Control, Hokkaido University Hospital, Sapporo, Japan, 5Depatment of Respiratory Medicine, Hokkaido Univ Faculty of Medicine and Graduate School of Medicine, Sapporo, Japan.
Introduction: Mycoplasma pneumoniae pneumonia (MPP) is often described as a self-limited disease. However, approximately 0.5-2% of all MPP cases present a fulminant course. The prevalence of macrolide-resistant MPP has emerged in several western countries but considered to be rare, and adult case of fulminant MPP due to a macrolide-resistant strain has not been reported. Case: A 39-year-old woman was admitted to a local general hospital owing to a progressive fever and malaise. On admission, her chest X-ray showed consolidation in her right lower lung field. She was clinically diagnosed as community-acquired pneumoniae and administration of ampicillin/sulbactam, at 6 g/day, and 2-g dose of azithromycin was given. On clinical day 7, her fever had not subsided, and the pulmonary lesions extended to both lung fields. Thus, bronchoalveolar lavage (BAL) was performed, but no specific diagnosis could be made. Owing to the extremely rapid progression, organizing pneumonia was considered, and treatment with prednisolone (PSL) was initiated at 40 mg/day from clinical day 7, and mPSL 1g/day was given on clinical days 11-13. However, neither her symptoms nor her pulmonary lesions improved, and hypoxemia emerged; therefore, she was transferred to our hospital. On clinical day 14, her indirect hemagglutination titer for M. pneumoniae had elevated to 1:2,560. From the clinical findings and clinical course, we diagnosed as fulminant MPP, and initiated levofloxacin at 500 mg/day and minomycin at 200 mg/day. Two days later, her symptoms and her pulmonary lesions improved. Because of the rarity of our patient’s clinical course, we performed further molecular identification from her BAL fluid. DNA of M. pneumoniae was identified by real-time polymerase chain reaction, and a mutation associated with resistance to macrolides at sites A2063G in the M. pneumoniae 23S rRNA gene domain was detected. Discussion: The host’s cellular hyper-immune response to M. pneumoniae is considered to play a central role in fulminant MPP. The reason macrolide-resistant MPP do not develop into severe infection was considered to be its less efficient protein synthesis due to a point mutation within its rRNA. Because M. pneumoniae has only one operon for constructing ribosomes, a point mutation in rRNA strain might affect ribosomal activity. Considering clinical course, we speculate that hyper-immune activity did not play a critical role in this case[MS1] , and the treatment for suppressing M. pneumoniae proliferation was indispensable. Conclusion: We report the first case of fulminant MPP caused by a macrolide-resistant strain in an adult.