β -Lactam antibiotics are first-line agents for the treatment and prevention of group B Streptococcus (GBS) infections. We previously reported clinical GBS isolates with reduced β -lactam susceptibility (GBS-RBS) and characterized them as harbouring amino acid substitutions in penicillin-binding proteins (PBPs). However, to our knowledge, GBS-RBS clinical isolates have never previously been isolated from pregnant women worldwide. We obtained 477 clinical GBS isolates from vaginal/rectal swabs of 4530 pregnant women in Japan. We determined the MICs of seven β -lactams for all 477 clinical isolates. Five clinical isolates showed reduced ceftibuten susceptibility. For these isolates, we performed sequencing analysis of pbp genes. None of the 477 isolates were non-susceptible to penicillin G, ampicillin, and meropenem. For five isolates, the MICs of ceftibuten were relatively high (64–128 μg/ml). Each of these isolates possessed a single amino acid substitution in PBP2X, and some of the substitutions had been previously found in GBS with reduced penicillin susceptibility. This is the first report of the isolation of clinical GBS-RBS isolates harbouring amino acid substitutions in PBP2X that confer reduced ceftibuten susceptibility from pregnant women.

Streptococcus agalactiae (Group B Streptococcus, GBS) is a pathogen which causes neonatal sepsis, meningitis, and invasive infections in the elderly and people with medical conditions (1,2). Although β-lactams are prescribed as first line drugs for the treatment and prevention of GBS infections, in case of patients with penicillin-allergies, macrolides and lincosamides are often prescribed for the same (1,2). However, macrolide and lincosamide resistance rates in GBS have been increasing worldwide (3-5). Macrolide resistant Streptococcus spp. has the following 2 major phenotypes: macrolides, lincosamides, streptogramin B (MLSB) and M (6,7). The MLSB phenotype confers a broad resistance to macrolides, lincosamides, and streptogramin B, whereas the M phenotype confers resistance to macrolides, but not to lincosamides and streptogramin B. In addition, an L phenotype also exists, which confers resistance to lincosamides, but not to macrolides (7). A macrolide resistance gene (erm) encoding erythromycin ribosomal methylase, confers typical MLSB phenotype (8). However, in the present study, 3 clinical ermB-PCR-positive isolates of GBS with L phenotype were isolated in Korea and the mechanisms

Spontaneous preterm birth is often caused by chorioamnionitis. Toll-like receptors (TLRs) have a role in the response of the innate immune system. The role of TLR5 in chorioamnionitis remains unclear: however, TLR5 was reported to have a significantly stronger effect on the induction of interleukin (IL)-6 when compared with other TLRs in amniotic epithelial cells. The aim of this study was to investigate TLR5 expression in placentas with preterm histologic chorioamnionitis (HCA). The expression levels of TLR5 were evaluated in the amnions, chorions, deciduae and villi with and without HCA using immunohistochemistry. The co-localization of IL-6 or IL-8 with TLR5 was examined by immunofluorescence. The production of IL-6 was examined in primary tissue cultured fetal membranes treated with and without the TLR5 agonist. The protein expression of TLR5 was significantly increased in amnions with HCA (p<0.05) and showed a trend toward an increase in chorions with HCA, whereas no significant difference was detected in the villi and decidua. TLR5 co-localized with IL-6 and IL-8 in amnions and chorions. IL-6 showed a significant increase (p<0.05) with the TLR5 agonist. These results suggest that TLR5 plays a role in the pathogenesis of preterm HCA and IL-6 production.

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