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Alterations of pbp1a, pbp2b, and pbp2x in Streptococcus pneumoniae isolates from children with otolaryngological infectious disease in the Sapporo district of Japan

  • ORIGINAL ARTICLE
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Journal of Infection and Chemotherapy

Abstract

Evaluation of beta-lactam susceptibility and polymerase chain reaction (PCR)-based genotyping of penicillin-binding proteins (PBP) 1A, 2B, and 2X were performed for Streptococcus pneumoniae isolates from children with otolaryngological infectious disease in the Sapporo district, Hokkaido Prefecture, Japan. Of 174 S. pneumoniae isolates, 14 (8%) were penicillin-resistant S. pneumoniae (PRSP), 87 (50%) were penicillin-intermediately-resistant, and 73 (42%) were penicillin-sensitive. Seventy-six (44%) had alterations in all of the three genes examined (pbp1a, pbp2b, and pbp2x), 81 (47%) had alterations in one or two of the genes, and 17 (10%) had no alterations. Isolates with alterations in all three genes showed low susceptibility to penicillin, while, in contrast, isolates with no alteration showed relatively high susceptibility to penicillin. Similar relationships were observed for other beta-lactams. The prevalence of PRSP in our study ranged from 5% to 12.8% (average, 8%), and there was much variation in the prevalence of PBP gene alterations among the cities. The results suggest that local differences in patterns of PBP gene alterations can be observed even at the district level. PCR-based genotyping of PBP genes is rapid, convenient, and useful to investigate genetic susceptibility to beta-lactams. Further, not only nationwide or prefectural surveys but also local surveillance at the district level is important for determining antimicrobial susceptibility status in daily practice.

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Correspondence to Atsushi Harimaya.

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A. Harimaya and S. Yokota contributed equally to this work.

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Harimaya, A., Yokota, Si., Sato, K. et al. Alterations of pbp1a, pbp2b, and pbp2x in Streptococcus pneumoniae isolates from children with otolaryngological infectious disease in the Sapporo district of Japan. J Infect Chemother 12, 366–371 (2006). https://doi.org/10.1007/s10156-006-0473-8

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  • DOI: https://doi.org/10.1007/s10156-006-0473-8

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