Erythromycin-Susceptible but Clindamycin-Resistant Phenotype of Clinical ermB-PCR-Positive Group B Streptococci Isolates with IS1216E-Inserted ermB.

Streptococcus agalactiae (Group B Streptococcus, GBS) is a pathogen which causes neo natal sepsis, meningitis, and invasive infections in the elderly and people with medical conditions. Macrolide and lincosamide resistance rates of GBS strains have been increasing worldwide. A macrolide resistance gene, erythromycin ribosomal methylase (erm), typically confers macrolides, lincosamides, streptogramin B resistance phenotype. However, in the current study, we recovered and characterized 3 clinical ermB-PCR-positive isolates of GBS with L phenotype. The presence of ermB and lnuB (lincosamide nucleotidyltransferase) genes in all 3 clinical isolates was confirmed using PCR. The ermB gene of the clinical isolates harbored C222T (N74N), T224C (I75T), and A299G (N100S) nucleotide (amino acid) substitutions, and insertion of an IS1216E element at nucleotide position 643, resulted in the deletion of a segment spanning nucleotides 643-738 of ermB gene, which suggested the loss-of-function of ErmB protein in the 3 clinical isolates. Since these clinical isolates show positive PCR result for a drug resistance gene despite its partial deletion, these results contradict their drug resistance phenotype. These factors must be considered while performing PCR-based detection of antimicrobial drug resistance genes.

Isolation of group B Streptococcus with reduced ß-lactam susceptibility from pregnant women.

ß-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 ß-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 ß-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.

The expression of Toll-like receptor 5 in preterm histologic chorioamnionitis.

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.