The affinity of [ 3 H]benzylpenicillin for penicillin-binding protein (PBP) 3A was reduced in 25 clinical isolates of -lactamase-negative ampicillin (AMP)-resistant (BLNAR)Haemophilus influenzae for which the AMP MIC was >1.0 g/ml. The affinities of PBP 3B and PBP 4 were also reduced in some strains. The sequences of the ftsI gene encoding the transpeptidase domain of PBP 3A and/or PBP 3B and of the dacB gene encoding PBP 4 were determined for these strains and compared to those of AMP-susceptible Rd strains. The BLNAR strains were classified into three groups on the basis of deduced amino acid substitutions in the ftsI gene, which is thought to be involved in septal peptidoglycan synthesis. His-517, near the conserved Lys-ThrGly (KTG) motif, was substituted for Arg-517 in group I strains (n ؍ 9), and Lys-526 was substituted for Asn-526 in group II strains (n ؍ 12). In group III strains (n ؍ 4), three residues (Met-377, Ser-385, and Leu-389), positioned near the conserved Ser-Ser-Asn (SSN) motif, were replaced with Ile, Thr, and Phe, respectively, in addition to the replacement with Lys-526. The MICs of cephem antibiotics with relatively high affinities for PBP 3A and PBP 3B were higher than those of AMP and meropenem for group III strains. The MICs of -lactams for H. influenzae transformants into which the ftsI gene from BLNAR strains was introduced were as high as those for the donors, and PBP 3A and PBP 3B showed decreased affinities for -lactams. There was no clear relationship between 7-bp deletions in the dacB gene and AMP susceptibility. Even though mutations in another gene(s) may be involved in -lactam resistance, these data indicate that mutations in the ftsI gene are the most important for development of resistance to -lactams in BLNAR strains.Haemophilus influenzae is one of the important pathogens causing respiratory tract infection (RTI), acute otitis media (AOM), pneumonia, and purulent meningitis. Ampicillin (AMP) resistance in this organism is due to two well-known mechanisms. One is resistance mediated by the production of TEM-1 (20) and ROB-1 (13) -lactamases, and the other is decreasing affinity of AMP for penicillin-binding proteins (PBPs) involved in peptidoglycan synthesis (14)(15)(16)19). Strains with resistance due to the latter mechanism are termed -lactamase-negative AMP-resistant (BLNAR) H. influenzae.In surveillance studies conducted in the United States the incidence of -lactamase-producing AMP-resistant (BLPAR) H. influenzae has gradually increased (6, 7, 10) and accounted for 36.4% of all isolates (5) in 1994 and 1995. In contrast, BLNAR isolates remain extremely uncommon in the United States.In Japan, according to nation wide surveillance studies conducted in 1997 and 1998, the proportion of clinical isolates supposed to be BLNAR has rapidly increased to 28.8% in parallel with the increased prevalence of penicillin (PEN)-resistant Streptcoccus pneumoniae. The characteristic of resistant H. influenzae isolates is that the AMP MIC is Ն1 g/ml, whereas the MIC for susce...
A continuous noninvasive method of systolic blood pressure estimation is described. Systolic blood pressure is estimated by combining two separately obtained components: a higher frequency component obtained by extracting a specific frequency band of pulse arrival time and a lower frequency component obtained from the intermittently acquired systolic blood pressure measurements with an auscultatory or oscillometric system. The pulse arrival time was determined by the time interval from QRS apex in electrocardiogram to the onset of photoplethysmogram in a fingertip beat-by-beat via an oximetric sensor. The method was examined in 20 patients during cardiovascular surgery. The estimated values of systolic blood pressure were compared with those measured invasively using a radial arterial catheter. The results showed that the correlation coefficients between estimated values and invasively obtained systolic blood pressure reached 0.97 +/- 0.02 (mean +/- SD), and the error remained within +/- 10% in 97.8% of the monitoring period. By using a system with automatic cuff inflation and deflation to acquire intermittent systolic blood pressure values, this method can be applicable for the continuous noninvasive monitoring of systolic blood pressure.
The prevention of dental caries and periodontal diseases is targeted at the control of dental plaque. In this context, chemical agents could represent a valuable complement to mechanical plaque control. The active agents should prevent biofilm formation without affecting the biological equilibrium within the oral cavity. Depending on the goals of the preventive measures, various strategies may be considered. Anti-plaque agents with properties other than bactericidal or bacteriostatic activities may be used in primary prevention. In this approach, a modest antiplaque effect may be sufficient or even desirable, as it would decrease the side effects of the active agent. Antimicrobial agents are best indicated in secondary and tertiary prevention, as the objectives are to restore health and to prevent disease recurrence. The rational is to prevent or delay subgingival recolonization by pathogenic micro-organisms. The development of in vitro oral biofilm models certainly represents a major advance for studying and testing oral anti-plaque agents in recent years. The results of these studies have shown that chlorhexidine, hexetidine, delmopinol, amine fluoride/stannous fluoride, triclosan, phenolic compounds, among others, may inhibit biofilm development and maturation as well as affect bacterial metabolism.
The oral microbiota change dramatically with each part of the oral cavity, even within the same mouth. Nevertheless, the microbiota associated with peri-implantitis and periodontitis have been considered the same. To improve our knowledge of the different communities of complex oral microbiota, we compared the microbial features between peri-implantitis and periodontitis in 20 patients with both diseases. Although the clinical symptoms of peri-implantitis were similar to those of periodontitis, the core microbiota of the diseases differed. Correlation analysis revealed the specific microbial co-occurrence patterns and found some of the species were associated with the clinical parameters in a disease-specific manner. The proportion of Prevotella nigrescens was significantly higher in peri-implantitis than in periodontitis, while the proportions of Peptostreptococcaceae sp. and Desulfomicrobium orale were significantly higher in periodontitis than in peri-implantitis. The severity of the peri-implantitis was also species-associated, including with an uncultured Treponema sp. that correlated to 4 clinical parameters. These results indicate that peri-implantitis and periodontitis are both polymicrobial infections with different causative pathogens. Our study provides a framework for the ecologically different bacterial communities between peri-implantitis and periodontitis, and it will be useful for further studies to understand the complex microbiota and pathogenic mechanisms of oral polymicrobial diseases.
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