Dental plaque samples from 40 children were screened for the presence of bacteria resistant to amoxicillin. Fifteen children had used amoxicillin and 25 had not used any antibiotic in the 3 months prior to sample collection. All (100%) of the children harbored amoxicillin-resistant oral bacteria. The median percentage of the total cultivable oral microbiota resistant to amoxicillin was 2.4% (range, 0.1 to 14.3%) in children without amoxicillin use and 10.9% (range, 0.8 to 97.3%) in children with amoxicillin use, with the latter value being significantly higher (P < 0.01). A total of 224 amoxicillin-resistant bacteria were isolated and comprised three main genera: Haemophilus spp., Streptococcus spp., and Veillonella spp. The biodiversity of the amoxicillinresistant microbiota was similar among the isolates from children with and without previous antibiotic use. The amoxicillin MIC at which 90% of the isolates were inhibited for isolates from children who had used amoxicillin in the previous 3 months was higher (64 mg liter ؊1 ) than that obtained for the isolates from subjects who had not used antibiotics (16 mg liter ؊1 ). The majority of the amoxicillin-resistant isolates (65%) were also resistant to at least one of the three antibiotics tested (penicillin, erythromycin, and tetracycline), with resistance to penicillin (51% of isolates) being the most frequently encountered. However, significantly more (P < 0.05) of the amoxicillin-resistant isolates from subjects with previous amoxicillin use were also resistant to erythromycin. This study has demonstrated that a diverse collection of amoxicillin-resistant bacteria is present in the oral cavity and that the number, proportions, MICs, and resistance to erythromycin can significantly increase with amoxicillin use.

We have characterized a transferable tetracycline resistance (Tc r ) element from a Streptococcus intermedius isolate. The gene responsible for this resistance was identified by PCR and Southern hybridization as tet(S). Furthermore, the genetic support for this determinant was shown to be a conjugative transposon closely related to Tn916. This element has been designated Tn916S.

The prevalence of tetracycline-resistant oral bacteria in healthy 4- and 6-year-old children who had not received antibiotics during the 3 months prior to sampling was investigated. Of the 47 children sampled, 46 harboured tetracycline-resistant bacteria. The median proportion of cultivable anaerobic and aerobic oral bacteria resistant to tetracycline was 1.1% and the MIC50 of these was 64 microg ml(-1). The majority (56%) of tetracycline-resistant bacteria were resistant to at least one other antibiotic, usually erythromycin. The most commonly identified tetracycline-resistant bacteria were the oral streptococci (65%), the next most prevalent groups were Veillonella spp. (10%) and Neisseria spp. (9%). The most frequently identified tetracycline resistance determinant was tet(M). The results of this study have shown that tetracycline-resistant oral bacteria were widespread amongst the children studied.

The results of this study show that tetracycline-resistant bacteria and tet(M) are maintained within the indigenous oral microbiota of children, even though they are unlikely to have been directly exposed to tetracycline.

tet(32) was identified in three bacterial isolates and in metagenomic DNA from the human oral cavity. The regions immediately flanking the gene were found to have similarities to the mobile elements TnB1230 from Butyrivibrio fibrisolvens, ATE-3 from Arcanobacterium pyogenes, and CTn5 from Clostridium difficile.Tetracycline resistance in the oral cavity is primarily mediated through the acquisition of genes encoding ribosomal protection proteins (RPPs) (5, 10, 13), which are often associated with mobile elements (9).The RPP gene tet(32) was initially reported in the Clostridium-related human colonic anaerobe K10 (4) but was subsequently reported to be a mosaic, tet(O/32/0) (12). Recently, the proposed nonmosaic sequence of tet(32) has been reported (6). In this study we characterize two variants of tet (32) and their immediate flanking regions.The strains and plasmids used in this study are shown in Table 1. Streptococcus salivarius FStet12 was isolated from a Finnish volunteer as part of a European study investigating antibiotic resistance in oral bacteria (ARTRADI; http://www .microfun.u-psud.fr/microfun/) and is the same isolate investigated by Patterson et al. (6). A tet(32) gene was cloned into pCC1BAC (Epicentre, Madison, WI) from metagenomic DNA isolated from saliva from healthy English volunteers (Table 1).The sequences of tet(32) and its flanking regions were obtained using single-specific-primer PCR and a primer-walking strategy ( Table 2). Analysis of the predicted amino acid sequences revealed two variants of Tet(32). The first, carried by 41.2T.2 and FStet12, shares 98% amino acid identity with the second variant carried by both 41.1T and ES2-K21. Interestingly, 41.1T and 41.2T.2A were isolated from the same subject (3), indicating that variants of Tet(32) can coexist. Tet(32) shows 69% amino acid identity with its closest relatives, Tet(M) in Tn916 and Tet(O) from Streptococcus pneumoniae (Fig. 1).Genomic DNA from the three isolates, together with the DNA of pPJW1, was used as template in a PCR using the degenerate RPP primers RPP-F and RPP-R (see Fig. 2 for the primer binding sites). Sequence analysis of the PCR products showed that only tet(32) was amplified, indicating the absence of other RPP genes.The presence of both variants of tet(32) in metagenomic DNA from Finland, Norway, and Scotland was demonstrated (data not shown) by PCR with specific primers, Tet(32) 21-F and Tet(32) 1898-R (Table 2). In addition, the input DNA used to make the clone ES2-K21 plus strains 41.1T and 41.2T.2 was derived from saliva taken from volunteers from England, demonstrating that tet(32) is present in different geographical locations within Europe.Analysis of the flanking regions revealed that those from 41.2T.2 and FStet12 are identical, suggesting that tet(32) may be contained on a region of mobile DNA. The flanking regions in 41.1T and ES2-K21 shared 99% nucleotide homology over

No abstract

Owing to a reputation for long lifetimes and excellent cycle stability, degradation in supercapacitors has largely been overlooked. In this work, we demonstrate that significant degradation in some commercial supercapacitors can in fact occur early in their life, leading to a rapid loss in capacitance, especially when utilized in full voltage range, high charge‐discharge frequency applications. By using a commercial 300 F lithium‐ion pseudocapacitor rated for 100,000 charge/discharge cycles as an example system, it is shown that a ∼96 % loss in capacitance over the first ∼2000 cycles is caused by significant structural and chemical change in the cathode active material (LiMn2O4, LMO). Multi‐scale in‐situ and ex‐situ characterization, using a combination of X‐ray computed tomography, Raman spectroscopy and X‐ray photoelectron spectroscopy, shows that while minimal material loss (∼5.5 %), attributed to the dissolution of Mn2+, is observed, the primary mode of degradation is due to manganese charge disproportionation (Mn3+→Mn4++Mn2+) and its physical consequences (i. e. microstrain formation, particle fragmentation, loss of conductivity etc.). In contrast to prior understanding of LMO material degradation in battery systems, negligible contributions from cubic‐to‐tetragonal phase transitions are observed. Hence, as supercapacitors are becoming more widely utilized in real‐world applications, this work demonstrates that it is vital to understand the mechanisms by which this family of devices change during their lifetimes, not just for lithium‐ion pseudocapacitors, but for a wide range of commercial chemistries.