85 research outputs found

    The role of beta-lactamase-producing-bacteria in mixed infections

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    Beta-lactamase-producing bacteria (BLPB) can play an important role in polymicrobial infections. They can have a direct pathogenic impact in causing the infection as well as an indirect effect through their ability to produce the enzyme beta-lactamase. BLPB may not only survive penicillin therapy but can also, as was demonstrated in in vitro and in vivo studies, protect other penicillin-susceptible bacteria from penicillin by releasing the free enzyme into their environment. This phenomenon occurs in upper respiratory tract, skin, soft tissue, surgical and other infections. The clinical, in vitro, and in vivo evidence supporting the role of these organisms in the increased failure rate of penicillin in eradication of these infections and the implication of that increased rate on the management of infections is discussed

    Biological foundation for periodontitis as a potential risk factor for atherosclerosis

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    Links between periodontal diseases and systemic diseases have been well documented by epidemiological studies. Recently, research has shifted to elucidating the biologic mechanism for a causal relationship. One focus of interest is atherosclerosis, the underlying event of cardiovascular diseases due to its serious health impact. However, it is still not clear whether periodontopathic pathogens are truly etiologic agents or ubiquitous bystanders. This article reviews the current understanding about the molecular biological interactions between periodontal disease and atherosclerosis and the biological plausibility of periodontitis as a potential risk factor for cardiovascular disease. Materials and methods:  The current literature regarding periodontal diseases and atherosclerosis and coronary vascular disease was searched using the Medline and PubMed databases. Results:  In vitro experiments and animal models are appropriate tools to investigate the biological interactions between periodontal disease and atherosclerosis at the cell molecular level. The concepts linking both pathologies refer to inflammatory response, immune responses, and hemostasis. In particular, Porphyromonas gingivalis appears to have unique, versatile pathogenic properties. Whether or not these findings from isolated cells or animal models are applicable in humans with genetic and environmental variations is yet to be determined. Likewise, the benefit from periodontal therapy on the development of atherosclerosis is unclear. Approaches targeting inflammatory and immune responses of periodontitis and atherosclerosis simultaneously are very intriguing. Conclusion:  An emerging concept suggests that a pathogenic burden from different sources might overcome an individual threshold culminating in clinical sequela. P. gingivalis contributes directly and indirectly to atherosclerosis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66109/1/j.1600-0765.2004.00771.x.pd

    The thrombotic potential of oral pathogens

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    In recent times the concept of infectious agents playing a role in cardiovascular disease has attracted much attention. Chronic oral disease such as periodontitis, provides a plausible route for entry of bacteria to the circulation. Upon entry to the circulation, the oral bacteria interact with platelets. It has been proposed that their ability to induce platelet aggregation and support platelet adhesion is a critical step in the pathogenesis of the infection process. Many published studies have demonstrated multiple mechanisms through which oral bacteria are able to bind to and activate platelets. This paper will review the various mechanisms oral bacteria use to interact with platelets

    Comparing very low birth weight versus very low gestation cohort methods for outcome analysis of high risk preterm infants

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    © 2017 The Author(s). Background: Compared to very low gestational age (<32 weeks, VLGA) cohorts, very low birth weight (<1500 g; VLBW) cohorts are more prone to selection bias toward small-for-gestational age (SGA) infants, which may impact upon the validity of data for benchmarking purposes. Method: Data from all VLGA or VLBW infants admitted in the 3 Networks between 2008 and 2011 were used. Two-thirds of each network cohort was randomly selected to develop prediction models for mortality and composite adverse outcome (CAO: mortality or cerebral injuries, chronic lung disease, severe retinopathy or necrotizing enterocolitis) and the remaining for internal validation. Areas under the ROC curves (AUC) of the models were compared. Results: VLBW cohort (24,335 infants) had twice more SGA infants (20.4% vs. 9.3%) than the VLGA cohort (29,180 infants) and had a higher rate of CAO (36.5% vs. 32.6%). The two models had equal prediction power for mortality and CAO (AUC 0.83), and similarly for all other cross-cohort validations (AUC 0.81-0.85). Neither model performed well for the extremes of birth weight for gestation (<1500 g and ≥32 weeks, AUC 0.50-0.65; ≥1500 g and <32 weeks, AUC 0.60-0.62). Conclusion: There was no difference in prediction power for adverse outcome between cohorting VLGA or VLBW despite substantial bias in SGA population. Either cohorting practises are suitable for international benchmarking

    An outcome audit of the treatment of acute dentoalveolar infection: impact of penicillin resistance

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    OBJECTIVES: The aim of this audit was to measure the outcome of treatment of acute dentoalveolar infection and to determine if this was influenced by choice of antibiotic therapy or the presence of penicillin-resistance. SUBJECTS AND METHODS: A total of 112 patients with dentoalveolar infection were included in the audit. All patients underwent drainage, either incisional (n=105) or opening of the pulp chamber (n=7) supplemented with antibiotic therapy. A pus specimen was obtained from each patient for culture and susceptibility. Clinical signs and symptoms were recorded at the time of first presentation and re-evaluated after 48 or 72 h. RESULTS: A total of 104 (99%) of the patients who underwent incisional drainage exhibited improvement after 72 h. Signs and symptoms also improved in five of the seven patients who underwent drainage by opening of the root canal although the degree of improvement was less than that achieved by incisional drainage. Penicillin-resistant bacteria were found in 42 (38%) of the 112 patients in this study. Of the 65 patients who were given penicillin, 28 had penicillin-resistant bacteria. There was no statistical difference in the clinical outcome with regard to the antibiotic prescribed and the presence of penicillin-resistant bacteria. Strains of penicillin-resistant bacteria were isolated more frequently in patients who had previously received penicillin (p<0.05). CONCLUSION: Incisional drainage appeared to produce a more rapid improvement compared to drainage by opening of the root canal. The presence of penicillin-resistant bacteria did not adversely affect the outcome of treatment. The observations made support surgical drainage as the first principle of management and question the value of prescribing penicillin as part of treatment
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