Objective: To determine the mechanism of rifampicin resistance in Streptococcus pneumoniae in Taiwan. Methods: Rifampicin resistance was investigated with respect to the rpoB gene in 23 invasive S. pneumoniae isolates collected from 1996 to 2001. PCR and molecular typing were used for genetic and epidemiological analyses. Transformation was used to determine the functional gene for resistance. Results: Twenty-two of 23 isolates carried at least one mutation at either cluster I or III of rpoB; the most frequent mutation found in 21 isolates (91%) was histidine (H499) to asparagine or tyrosine at position 499, followed by isoleucine to valine (I624V) at position 624 in 16 isolates (70%), tyrosine to phenylalanine (Y589F) at position 589 in 14 isolates (60.9%) and isoleucine to valine (I608V) at position 608 in 13 isolates (56.5%). Less-frequent mutations were also identified: D489V, R597F, N623E, N623S, N669D, Q671K, Y674F and A683V. High-level rifampicin resistance was observed in isolates with a mutation at position 499 or 489. Mutations other than at position 499 or 489 played little role in or had no relation to rifampicin resistance. No dominant epidemic strain was observed with ribotyping, multilocus sequence typing, or serotyping. Conclusions: Rifampicin resistance among multidrug-resistant S. pneumoniae in Taiwan was mostly caused by rpoB mutations.
