Background-Antibiotic prophylaxis recommendations for the prevention of infective endocarditis are based in part on studies of bacteremia from dental procedures, but toothbrushing may pose a greater threat. The purpose of this study was to compare the incidence, duration, nature, and magnitude of endocarditis-related bacteremia from single-tooth extraction and toothbrushing and to determine the impact of amoxicillin prophylaxis on single-tooth extraction. Methods and Results-In this double-blind, placebo-controlled study, 290 subjects were randomized to (1) toothbrushing, (2) single-tooth extraction with amoxicillin prophylaxis, or (3) single-tooth extraction with identical placebo. Blood was drawn for bacterial culturing and identification at 6 time points before, during, and after these interventions. The focus of our analysis was on bacterial species reported to cause infective endocarditis. We identified 98 bacterial species, 32 of which are reported to cause endocarditis. Cumulative incidence of endocarditis-related bacteria from all 6 blood draws was 23%, 33%, and 60% for the toothbrushing, extraction-amoxicillin, and extraction-placebo groups, respectively (PϽ0.0001). Significant differences were identified among the 3 groups at draws 2, 3,4, and 5 (all PϽ0.05). Amoxicillin resulted in a significant decrease in positive cultures (PϽ0.0001). Conclusions-Although amoxicillin has a significant impact on bacteremia resulting from a single-tooth extraction, given the greater frequency for oral hygiene, toothbrushing may be a greater threat for individuals at risk for infective endocarditis. (Circulation. 2008;117:3118-3125.)
Background Infective endocarditis (IE) often is caused by bacteria that colonize teeth. The authors conducted a study to determine if poor oral hygiene or dental disease are risk factors for developing bacteremia after toothbrushing or single-tooth extraction. Methods One hundred ninety-four participants in a study were in either a toothbrushing group or a single-tooth extraction with placebo group. The authors assessed the participants’ oral hygiene, gingivitis and periodontitis statuses. They assayed blood samples obtained before, during and after the toothbrushing or extraction interventions for IE-associated bacteria. Results The authors found that oral hygiene and gingival disease indexes were associated significantly with IE-related bacteremia after toothbrushing. Participants with mean plaque and calculus scores of 2 or greater were at a 3.78- and 4.43-fold increased risk of developing bacteremia, respectively. The presence of generalized bleeding after toothbrushing was associated with an almost eightfold increase in risk of developing bacteremia. There was no significant association between any of the measures of periodontal disease and the incidence of bacteremia after toothbrushing. The oral hygiene or disease status of a tooth was not significantly associated with bacteremia after its extraction. Conclusion Bacteremia after toothbrushing is associated with poor oral hygiene and gingival bleeding after toothbrushing. Clinical Implications Improvements in oral hygiene may reduce the risk of developing IE.
Type 1 fimbriae and extracellular polysaccharides are preeminent uropathogenic Escherichia coli virulence determinants in the murine urinary tract the E. coli K-12 strain. Mutations in type 1 fimbrial genes resulted in severely attenuated colonization, even in the case of a mutant with an insertion upstream of the fim operon that affected the rate of fimbrial switching from the 'off' to the 'on' phase. Three mutants had insertions in a new type II capsule biosynthesis locus on a pathogenicity island and were impaired in the production of capsule in vivo. An additional mutant with an insertion in wecE was unable to synthesize enterobacterial common antigen. These results confirm the pre-eminence of type 1 fimbriae, establish the importance of extracellular polysaccharides in the pathogenesis of UTI and identify new urovirulence determinants. IntroductionThe urinary tract is a normally sterile system that is protected from the nearby colonic microflora by non-specific defences including the epithelial barrier, the antibacterial properties of the bladder mucosa and the flow of urine. Nevertheless, urinary tract infections (UTIs) are among the most common infectious diseases, affecting a wide range of individuals including preschool girls, women of childbearing age and the elderly (Warren, 1996). These infections usually result from the entry of periurethral microorganisms through the urethra into the bladder lumen. The bacteria may ascend further via the ureters into the kidneys and even breach the kidney parenchyma to enter the lymphatic system or the bloodstream. Therefore, the manifestations of UTIs can range from asymptomatic bacteriuria to urethritis, cystitis, pyelonephritis, bacteraemia and sepsis (Warren, 1996).Escherichia coli is by far the most common uropathogen. Reports of dramatic outbreaks of nosocomial and community-acquired pyelonephritis and cystitis involving single clones of E. coli (Tullus et al., 1984;Phillips et al., 1988;Kunin et al., 1993;Manges et al., 2001) emphasize the fact that certain strains are uniquely equipped to infect the urinary tract. Such uropathogenic E. coli (UPEC) strains may belong to specific lineages among specific serogroups (Arbeit et al., 1990;Johnson et al., 1997;Zhang et al., 1997). The concept that certain traits are more common among E. coli isolated from patients with UTIs than among other E. coli strains is well SummaryEscherichia coli is the leading cause of urinary tract infections (UTIs). Despite the association of numerous bacterial factors with uropathogenic E. coli (UPEC), few such factors have been proved to be required for UTI in animal models. Previous investigations of urovirulence factors have relied on prior identification of phenotypic characteristics. We used signature-tagged mutagenesis (STM) in an unbiased effort to identify genes that are essential for UPEC survival within the murine urinary tract. A library of 2049 transposon mutants of the prototypic UPEC strain CFT073 was constructed using mini-Tn5km2 carrying 92 unique tags and screened in ...
Trauma intensive care unit (TICU) patients requiring mechanical respiratory support frequently develop ventilator-associated pneumonia (VAP). Oral and oropharyngeal bacteria are believed to be responsible for many cases of VAP, but definitive evidence of this relationship is lacking. Earlier studies used conventional culture-based methods for identification of bacterial pathogens, but these methods are insufficient, as some bacteria may be uncultivable or difficult to grow. The purpose of this study was to use a culture-independent molecular approach to analyze and compare the bacterial species colonizing the oral cavity and the lungs of TICU patients who developed VAP. Bacterial samples were acquired from the dorsal tongue and bronchoalveolar lavage fluid of 16 patients. Bacterial DNA was extracted, and the 16S rRNA genes were PCR amplified, cloned into Escherichia coli, and sequenced. The sequencing data revealed the following: (i) a wide diversity of bacterial species in both the oral and pulmonary sites, some of them novel; (ii) known and putative respiratory pathogens colonizing both the oral cavity and lungs of 14 patients; and (iii) a number of bacterial pathogens (e.g., Dialister pneumosintes, Haemophilus segnis, Gemella morbillorum, and Pseudomonas fluorescens) in lung samples that had not been reported previously at this site when culture-based methods were used. Our data indicate that the dorsal surface of the tongue serves as a potential reservoir for bacterial species involved in VAP. Furthermore, it is clear that the diversity of bacterial pathogens for VAP is far more complex than the current literature suggests.Ventilator-associated pneumonia (VAP) frequently occurs in patients requiring mechanical respiratory support, with incidence from 8% to 28% and mortality rates from 24% to 76%, depending on the population studied and the techniques used for the diagnosis of pneumonia (3). VAP is often associated with prolonged hospitalization of trauma patients, which can result in additional hospital charges of about $40,000 per patient (1).The etiology of VAP is variable, depending on the time of onset, duration of hospitalization, population studied, and hospital setting (3). For example, Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae usually predominate in early-onset VAP. Aerobic gram-negative bacteria, including members of the family Enterobacteriaceae, have been isolated in both early-and late-onset pneumonia. Pseudomonas aeruginosa and Acinetobacter and Enterobacter species are often isolated from late-onset pneumonia. Trauma intensive care unit (TICU) patients are at high risk of infection with S. aureus, among a variety of other microorganisms. In the postsurgical population, H. influenzae and S. pneumoniae dominate in trauma patients but not in patients with other diagnoses (3, 5). In one study, oral anaerobic bacteria such as Prevotella, Veillonella, and Fusobacterium spp. were isolated from VAP patients (4).Several different routes of infection by VAP pathogens hav...
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