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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infective endocarditis represents one of the few potentially fatal infections that may be caused in the patient by a dentist. Efforts to reduce the incidence of this disease usually take the form of appropriate antibiotic cover prior to dental treatment, together with the establishment and maintenance of good oral health. This paper is a report of a survey on the dental health and awareness of 81 'at-risk' patients attending a cardiology outpatient clinic. It was found that whilst the patients were apparently well motivated and well informed, a high prevalence of periodontal disease existed in the group. It is concluded that when patients are diagnosed with a cardiac disorder which predisposes to infective endocarditis they should have a dental examination as soon as possible, preferably by a dentist experienced in the treatment of patients with special needs.
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PMID:The dental status and attitudes of patients at risk from infective endocarditis. 842 17

Infective endocarditis refers to infection of the endocardium or heart valves by microbes, resulting in tissue destruction. Clinical presentation is quite variable, and a high level of suspicion is essential for recognition. Diagnosis is dependent on identification of the causative agent in blood cultures. Cultures that are persistently negative indicate the presence of culture-negative endocarditis, and diagnosis is one of exclusion. Treatment of endocarditis consists of high doses of antibiotics active against the infecting organism. Individualized therapy is the key to management.
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PMID:Endocarditis. Changing trends in epidemiology, clinical and microbiologic spectrum. 846 80

Infective endocarditis begins with adherence of microorganisms to cardiac tissues. These tissues have often been previously damaged, creating a thrombotic lesion consisting of platelets and fibrin. Circulating microorganisms localize to this lesion. The tissue specificity of endocarditis likely results from interactions between cell-surface determinants on the endocardium, platelet, and microorganism. Interference with these binding events may offer a means of modifying the course of the infection.
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PMID:Adherence events in the pathogenesis of infective endocarditis. 846 51

Infective endocarditis is a life-threatening disease which may be complicated by ring-valve abscess. Since this complication increases morbidity and mortality early diagnosis is important. Pericardial effusion complicating infective endocarditis is uncommon and should raise suspicion of the presence of an abscess. We describe 2 patients admitted for infective endocarditis and pericarditis. In both, ring-valve abscess was suspected on clinical grounds. At surgery there was pathological confirmation of the diagnosis. Both patients underwent successful aortic valve replacement with complete recovery. Controlled trials are providing increasing evidence for the superiority of transesophageal echocardiography in detecting valvular vegetations. Moreover, it is the most accurate means of detecting ring-valve abscess in cases of infective endocarditis. In view of these advantages, we propose the use of transesophageal echocardiography in every case of infective endocarditis.
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PMID:[Ring-valve abscess--a diagnostic challenge]. 849 34

Infective endocarditis is a rare, serious, and sometimes fatal heart disease that can be caused by bacteremia from the mouth, especially by Streptococcus viridans. As a result, dental procedures have often been blamed for cases of infective endocarditis but poor oral health and hygiene may actually cause more cases of infective endocarditis than do dental procedures. The American Heart Association and other groups have published recommendations for the prevention of infective endocarditis in dental patients and advise specific antibiotic regimens for certain dental procedures in cardiac-abnormal patients. The most recent (1990) American Heart Association recommendations are the most conservative yet, reflecting concern about the prevention of not only infective endocarditis, but also problems resulting from the antibiotics themselves. Clinicians should carefully consider not only the patient's medical history, but also the types of dental procedures planned.
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PMID:Prevention of infective endocarditis: an update for clinicians. American Heart Association. 851 Dec 76

Infective endocarditis is a rare but important complication of certain types of dental treatment. Antibiotic prophylaxis is routinely prescribed for patients with known congenital heart disease. In this report we describe two patients in whom endocarditis developed within 3 months of the dental procedure, despite appropriate antibiotics. Endocarditis should be actively excluded if patients develop a fever associated with non-specific symptoms following an 'at risk' dental procedure.
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PMID:Infective endocarditis in children following dental extraction and appropriate antibiotic prophylaxis. 879 41

Infective endocarditis, especially when it involves prosthetic valves, is a serious, often fatal illness. Although antibiotics are essential in management, surgery is required in many patients who develop even incipient heart failure and structural complications. Early identification and referral results in improved mortality and morbidity rates, and there is evidence that surgery should play a larger role in managing infective endocarditis. Patients with intracardiac pacemakers and cardioverting devices represent a growing reservoir of patients with the potential to develop endocarditis.
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PMID:Indications for and timing of surgical intervention in infective endocarditis. 885 33

Infective endocarditis remains a serious medical problem despite advancements in laboratory detection, echocardiographic techniques, and newer antibiotic agents. This article summarizes the microbial agents in infective endocarditis, in addition to developments in medical and antibiotic management.
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PMID:Advances in medical and antibiotic management of infective endocarditis. 885 34

Infective endocarditis is an uncommon disease but retains a high mortality. Glycopeptides are used for patients with resistant pathogens, those allergic to penicillins or for those outside the hospital. The once daily administration of teicoplanin and its low toxicity suggest that it would be suitable for use in the long courses required for endocarditis. However, the dosage and combinations to be used require further study. A retrospective review has been made of 104 episodes of endocarditis treated with teicoplanin in 101 patients seen over 7 years. Most patients had been referred to major London hospitals following failure of medical treatment. After three loading doses of 400 mg, teicoplanin was given at a dose of 400 mg/day in combination with other antibiotics such as gentamicin. Follow up was for one year. The most common pathogens were Streptococcus sanguis (15 cases), Staphylococcus aureus (13 cases) and Staphylococcus epidermidis (10 cases). Of 80 patients febrile at the start of treatment with teicoplanin, 63 (79%) lost their fever within a median of 2 days (1-35 days). Cure without surgery was effected in 50 (48%) and 75% of patients survived. Other antibiotics, usually gentamicin or rifampicin, were used in 92 (90%) of patients. Two strains of Streptococcus spp. were said to be resistant but there was no relationship between MIC of teicoplanin and outcome. Pathogens with a high MBC tended to be more likely to resist treatment. Adverse effects resulted in the withdrawal of teicoplanin in 20 cases (19%) but most events were mild and renal deterioration occurred in only five patients. Teicoplanin was effective in the treatment of endocarditis and appeared to be safe given the severity of disease in the patients treated.
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PMID:Treatment of endocarditis with teicoplanin: a retrospective analysis of 104 cases. 888 25

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


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