Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral streptococci may cause infective endocarditis in patients with susceptible cardiac disease after dental treatment. Multiple dental visits, each preceded by penicillin prophylaxis, may result in the unwanted development of resistant oral streptococci. This study was undertaken to determine whether resistant oral streptococci would develop after the repeated use of penicillin prophylaxis in healthy adults. Plaque samples were collected from 20 subjects on each Monday for 5 successive weeks. Each subject was administered 2 gm penicillin V followed by 1 gm 6 hours later (standard prophylaxis regimen of the American Heart Association), on three successive Mondays (weeks 2, 3, and 4). The total cultivable oral streptococci and penicillin-resistant oral streptococci were determined for each plaque sample, and representative colonies of resistant streptococci were speciated. During the study, there was a significant increase in the number of subjects who harbored penicillin-resistant oral streptococci. However, with the exception of one subject who had resistant streptococci throughout the study, the number of resistant strains represented only 0.0003% to 0.41% of the total cultivable oral streptococci.
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PMID:The development of penicillin-resistant oral streptococci after repeated penicillin prophylaxis. 214 41

Streptococcus mutans, a dental caries pathogen, also causes endocarditis and is detected in atheroscelerotic plaque. We investigated the potential for an invasive strain of S. mutans, OMZ175, to accelerate plaque growth in apolipoprotein E deficient (ApoE(null)) mice without and with balloon angioplasty (BA) injury, a model of restenosis. ApoE(null) mice were divided into 4 groups (N = 10), 2 with and 2 without BA. One each of the BA and non-BA groups was infected with S. mutans (Sm). S. mutans DNA, plaque area, inflammatory cell invasion, and Toll-like receptor (TLR) expression were measured at 6-20 weeks post-infection. S. mutans genomic DNA was detected in the aorta, liver, spleen, and heart. Plaque growth was significantly increased in infected mice with BA (Sm+BA) vs. those in the non-infected groups (p < 0.03). Plaque size was increased after infection without BA (Sm), but did not reach significance. Aortic specimens from both S. mutans and Sm+BA groups displayed increased numbers of macrophages, and TLR4 expression was increased in BA mice. In conclusion, S. mutans infection accelerated plaque growth, macrophage invasion, and TLR4 expression after angioplasty. S. mutans may also be associated with atherosclerotic plaque growth in non-injured arteries.
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PMID:Increased atherogenesis during Streptococcus mutans infection in ApoE-null mice. 2226 33

In order to determine whether adequate attention is paid to the maintenance of good oral health in patients at risk of developing infective endocarditis, we studied 44 black patients with severe rheumatic heart disease before they had cardiac surgery. Plaque and gingival index scores were calculated and panoramic radiographs were done in all patients. There were 17 males and 27 females (mean age: 30.6 years). The plaque and gingival index scores were classified as poor in 31.8 and 54.6% of patients, respectively. Panoramic radiographic findings included caries in 56.8% of patients, peri-apical pathology in 18.1% and retained roots in 22.7% of patients. This study demonstrates that inadequate attention is paid to the maintenance of good oral health in patients with severe rheumatic heart disease. The oral and dental care of patients at risk of developing infective endocarditis needs to be improved.
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PMID:Oral health of patients with severe rheumatic heart disease. 2283 56