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)

From August 1981 to July 1984, a total of 97 Hancock pericardial xenografts were implanted in 84 patients, whose ages ranged from 13 to 75 years (mean 55.7 +/- 13). Mitral value replacement was performed in 17, aortic valve replacement in 54, and mitral-aortic valve replacement in 13. Operative survivors were reevaluated from July to September 1985. Cumulative duration of follow-up is 167 patient-years (range 0.5 to 4.1 years), and follow-up is 99% complete. The overall late mortality (at 4 years) is 3.6% +/- 1.4% per patient year, and the actuarial survival rate is 95.4% +/- 3% for aortic valve replacement, 74.7% +/- 16.5% for mitral valve replacement, and 67.1% +/- 20.7% for mitral-aortic valve replacement. One patient sustained a thromboembolic event after mitral valve replacement, but no such complications occurred after aortic or mitral-aortic valve replacement. Actuarial freedom from embolism at 4 years is 100% for aortic and mitral-aortic valve replacement and 93.3% +/- 6.4% for mitral valve replacement. Reoperation for Hancock pericardial xenograft dysfunction was performed in seven patients (five aortic and two mitral-aortic). In the aortic valve replacement group the causes were endocarditis in one, paravalvular leak in one, and primary tissue failure in three; all survived reoperation. The two patients with mitral-aortic valve replacement required reoperation because of primary tissue failure of both Hancock pericardial xenografts, and one died. All values explanted because of primary tissue failure showed commissural tears causing severe prosthetic regurgitation. Calcium deposits were severe in one and mild but unrelated to the cusp rupture in another. Collagen disarray was seen only at the site of the tears, whereas the collagen structure was well preserved in the intact parts of the cusps. Four patients with aortic valve replacement and one with mitral valve replacement show evidence of Hancock pericardial xenograft failure and are awaiting reoperation. The actuarial freedom from primary tissue failure at 4 years is 74.3% +/- 9.8% for aortic and 78.9% +/- 13.2% for mitral Hancock pericardial xenografts. At medium-term follow-up, the Hancock pericardial xenograft has shown poor durability and an extremely high rate of early mechanical failure, especially in the aortic position. These observations suggest the need for a close follow-up of Hancock pericardial xenograft recipients and possibly elective reoperation in asymptomatic patients with clinical evidence of prosthetic failure. These results have led us to discontinue the clinical use of this pericardial xenograft.
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PMID:Early mechanical failures of the Hancock pericardial xenograft. 361 18

Infective endocarditis is characterized by the formation of septic masses of platelets on the surfaces of heart valves and is most commonly caused by viridans streptococci. Streptococcal virulence in endocarditis involves factors that promote infectivity and pathogenicity. Adhesins and exopolysaccharide (glycocalyx) contribute to infectivity. Although many factors may contribute to pathogenicity, the platelet aggregation-associated protein (PAAP) of Streptococcus sanguis contributes directly to the development of experimental endocarditis. PAAP is synthesized as a rhamnose-rich glycoprotein of 115 kDa and contains a collagen-like platelet-interactive domain, pro-gly-glu-gln-gly-pro-lys. Expressed on the cell wall of platelet aggregation-inducing strains (Agg+) of S. sanguis, PAAP apparently interacts with a signal-transducing receptor complex on platelets, which includes a novel 175-kDa alpha 2-integrin-associated protein and a 65-kDa collagen-binding component. From available data, the role of PAAP in the pathogenesis of experimental endocarditis may be explained by a proposed mechanistic model. On injured heart valves, PAAP first enhances platelet accumulation into a fibrin-enmeshed thrombus (vegetation), within which S. sanguis colonizes. Colonizing bacteria must resist platelet microbicidal protein (PMPR). The aggregation of platelets on the heart valve may be potentiated by an ectoATPase expressed on the surface of the S. sanguis and platelet alpha-adrenoreceptors that respond to endogenous catecholamines. The expression of PAAP may be modified during infection. Collagen is exposed on damaged heart valves; fever (heat shock) occurs during endocarditis. In response to heat shock or collagen in vitro, PAAP expression is altered. After colonization, streptococcal exotoxin(s) may cause fever. Proteases and other enzymes from streptococci and host sources may directly destroy the heart valves. When PAAP is unexpressed or neutralized with specific antibodies, experimental endocarditis runs a milder course and vegetations are smaller. The data suggest strongly, therefore, that the role of PAAP may overlap the colonization function of putative adhesins such as FimA or SsaB. Finally, PAAP also contributes to the development of the characteristic septic mural thrombus (vegetation) of infective endocarditis and the signs of valvular pathology.
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PMID:Platelet-streptococcal interactions in endocarditis. 890 79

The gram-negative fastidious human oropharyngeal Aggregatibacter actinomycetemcomitans is implicated in the etiology of infective endocarditis. EmaA, an oligomeric coiled-coil adhesin homologous to YadA of Yersinia enterocolitica, was hypothesized to mediate the interaction of A. actinomycetemcomitans with collagen. Collagen, the most abundant protein in human bodies and the main component of extracellular matrix (ECM), predominates in the supporting tissue of cardiac valves. To extend our earlier studies using purified collagen to determine bacterial binding activities, we developed a tissue model using rabbit cardiac valves to investigate the interaction of A. actinomycetemcomitans with native collagen. The resected mitral valves, with or without removal of the endothelium, were incubated with equivalent numbers of the wild type and the isogenic emaA mutant defective in collagen binding. There was no difference in binding between the wild-type and the mutant strains when the endothelium remained intact. However, the emaA mutant was fivefold less effective than the wild-type strain in colonizing the exposed ECM. A 10-fold increase in the binding of the wild-type strain to ECM was observed compared with the intact endothelium. Similar observations were replicated in an in vivo endocarditis rabbit model; the emaA mutant was 10-fold less effective in the initial infection of the traumatized aortic valve. Colocalization studies indicated that A. actinomycetemcomitans bound to type I collagen. A. actinomycetemcomitans preferentially colonized the ECM and, together with the evidence that EmaA interacts with the native collagen, suggested that the adhesin is likely a potential virulence determinant of the bacterium in the initiation of infective endocarditis.
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PMID:EmaA, a potential virulence determinant of Aggregatibacter actinomycetemcomitans in infective endocarditis. 1834 33

Streptococcus mutans is a major pathogen of dental caries. Collagen-binding proteins (CBPs) (approximately 120 kDa), termed Cnm and Cbm, are regarded as important cell surface antigens related to the adherence of S. mutans to collagenous tissue. Furthermore, CBP-positive S. mutans strains are associated with various systemic diseases involving bacteremia, such as infective endocarditis. Endodontic infection is considered to be an important cause of bacteremia, but little is known regarding the presence of S. mutans in dental pulp tissue. In the present study, the distribution and virulence of S. mutans in dental pulp tissues were investigated by focusing on CBPs. Adhesion and invasion properties of various S. mutans strains were analyzed using human dental pulp fibroblasts (HDPFs). CBP-positive strains had a significantly higher rate of adhesion to HDPFs compared with CBP-defective isogenic mutant strains (P<0.001). In addition, CBP-positive strains induced HDPF proliferation, which is a possible mechanism related to development of hyperplastic pulpitis. The distribution of S. mutans strains isolated from infected root canal specimens was then analyzed by PCR. We found that approximately 50% of the root canal specimens were positive for S. mutans. Approximately 20% of these strains were Cnm-positive, while no Cbm-positive strains were isolated. The Cnm-positive strains isolated from the specimens showed adhesion to HDPFs. Our results suggest that CBP-positive S. mutans strains exhibit high colonization in dental pulp. This could be a possible virulence factor for various systemic diseases.
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PMID:Contribution of the Collagen-Binding Proteins of Streptococcus mutans to Bacterial Colonization of Inflamed Dental Pulp. 2744 66