Nosocomial outbreak of telithromycin- and fluoroquinolone-resistant Streptococcus pneumoniae in a Japanese hospital
Abstract number: 1733_232
Muratani T., Kobayashi T., Matsumoto on behalf of the Hibiki Research Group for Clinical Microbiology T.
Background:Streptococcus pneumoniae is a major pathogen causing community-acquired pneumonia and acute bronchitis. Amoxicillin, macrolides, and fluoroquinolones have been used in clinically, because of their potent activity against S. pneumoniae. Recently, the resistant isolates to b-lactams including amoxicillin and macrolides, such as erythromycin, clarithromycin, rokitamycin, azithromycin have accounted for majority in clinical isolates. But telithromycin and fluoroquinolone have kept potent activity. We isolated high resistant isolates to telithromycin and fluoroquinolones in 2004 and 2006. The aim of the this study is to analyse these resistant isolates.
Materials and Methods: The resistant isolates to telithromycin and levofloxacin were isolated from 2 patients in 2004, and 9 patients in 2006 from a same hospital. The MICs of various antimicrobials against the isolates were determined by the two-fold serial agar dilution method. PCR and DNA sequencing technique were used to analyse mechanism of resistance to telithromycin. PFGE technique was performed to analyse clonal spread.
Results: The MICs of levofloxacin and telithromycin were 816 and 1632 mg/L, respectively. According to PCR results these isolates had ermB, but didn't have mefA, mefE, ermTR. The DNA sequence of 23S rRNA, rplD and rplV of these resistant isolates were the same as the susceptible strain. The ermB of resistant isolates had an amino acid change (Asn100Ser), and 1 or 2 mutations in upstream base sequence. PFGE technique using SmaI digested DNA of resistants was performed against 7 isolates. The results revealed the 7 resistant isolates were the same clone.
Conclusions: We isolated 11 telithromycin and fluoroquinolone high resistant S. pneumoniae. The mechanisms of resistance to telithromycin were considered mutated ermB with changed upstream base sequence. It was considered that the 11 resistant isolates were spread by nosocomial infection. We must minimise the spread of such resistant S. pneumoniae.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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