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Health care-associated IE refers to IE that develops in the context of recent contact with a health care setting, with onset of symptoms ≥48 hours after hospitalization.
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e exposure [1]. Community-associated IE refers to IE that develops in the absence of recent contact with a health care setting, with diagnosis established within 48 hours of hospital admission. <span>Health care-associated IE refers to IE that develops in the context of recent contact with a health care setting, with onset of symptoms ≥48 hours after hospitalization. Between 2000 and 2011, the incidence of IE in the United States increased from 11 per 100,000 population to 15 per 100,000 population [2,3]. The precise incidence of IE is difficult to




The precise incidence of IE is difficult to ascertain because case definitions have varied over time between authors and between clinical centers [4]. In addition, the incidence of predisposing conditions such as rheumatic heart disease or injection drug use is variable over time and between regions and in low- and high-income countries [5].
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h onset of symptoms ≥48 hours after hospitalization. Between 2000 and 2011, the incidence of IE in the United States increased from 11 per 100,000 population to 15 per 100,000 population [2,3]. <span>The precise incidence of IE is difficult to ascertain because case definitions have varied over time between authors and between clinical centers [4]. In addition, the incidence of predisposing conditions such as rheumatic heart disease or injection drug use is variable over time and between regions and in low- and high-income countries [5]. For example, the incidence of IE among patients admitted to Philadelphia-area hospitals from 1988 to 1990 was approximately 11.6 cases per 100,000 person-years [6]. In contrast, the inc




A population-based observational study in France in 2008 noted the annual incidence of IE was 33.8 cases per million [13]. The incidence was highest in men 75 to 79 years and the majority of patients had no known prior heart disease; health care-associated IE accounted for 27 percent of cases.
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idence of IE in women increased (from 1.4 to 6.7 cases/100,000 person-years). Other studies have reported incidence rates for IE ranging from 0.6 to 6.0 cases per 100,000 person-years [4,9-12]. <span>A population-based observational study in France in 2008 noted the annual incidence of IE was 33.8 cases per million [13]. The incidence was highest in men 75 to 79 years and the majority of patients had no known prior heart disease; health care-associated IE accounted for 27 percent of cases. Similarly, an observational study in Spain noted an increase in the incidence of IE between 2003 and 2014, from 2.72 to 3.49 per 100,000 person-years; the rise was higher among older ad




Age >60 years — More than half of all IE cases in the United States and Europe occur in patients over the age of 60; the median age has increased steadily during the past 40 years [12,15-17]. This trend is probably due to two factors: the decline in the incidence and importance of rheumatic heart disease as a risk factor for IE and the increasing proportion of older adult individuals in the general population. Older adults are more likely to develop degenerative valve disease and to require valve replacement, both of which are associated with an increased risk of IE.
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tions. Issues related to antimicrobial prophylaxis for prevention of IE are discussed separately. (See "Antimicrobial prophylaxis for the prevention of bacterial endocarditis".) Patient factors <span>Age >60 years — More than half of all IE cases in the United States and Europe occur in patients over the age of 60; the median age has increased steadily during the past 40 years [12,15-17]. This trend is probably due to two factors: the decline in the incidence and importance of rheumatic heart disease as a risk factor for IE and the increasing proportion of older adult individuals in the general population. Older adults are more likely to develop degenerative valve disease and to require valve replacement, both of which are associated with an increased risk of IE. Male sex — Men predominate in most case series of IE; male-to-female ratios range from 3:2 to 9:1 [12,18,19]. Injection drug use — Risk factors related to injection drug use include blo




Male sex — Men predominate in most case series of IE; male-to-female ratios range from 3:2 to 9:1 [12,18,19].
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iduals in the general population. Older adults are more likely to develop degenerative valve disease and to require valve replacement, both of which are associated with an increased risk of IE. <span>Male sex — Men predominate in most case series of IE; male-to-female ratios range from 3:2 to 9:1 [12,18,19]. Injection drug use — Risk factors related to injection drug use include bloodstream seeding with skin flora, oral flora, and/or organisms contaminating the drug or materials used for in




Injection drug use — Risk factors related to injection drug use include bloodstream seeding with skin flora, oral flora, and/or organisms contaminating the drug or materials used for injection [20]. In addition, some illicit drugs may induce valvular endothelial damage, predisposing to subsequent infection
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quire valve replacement, both of which are associated with an increased risk of IE. Male sex — Men predominate in most case series of IE; male-to-female ratios range from 3:2 to 9:1 [12,18,19]. <span>Injection drug use — Risk factors related to injection drug use include bloodstream seeding with skin flora, oral flora, and/or organisms contaminating the drug or materials used for injection [20]. In addition, some illicit drugs may induce valvular endothelial damage, predisposing to subsequent infection. Issues related to IE and injection drug use are discussed further separately. (See "Right-sided native valve infective endocarditis".) Poor dentition or dental infection — Poor dentiti




Poor dentition or dental infection — Poor dentition and/or dental infection are presumed to be risk factors for IE due to oral flora [21,22]. Routine dental cleaning is not a risk factor for IE; dental procedures that involve manipulation of gingival tissue or the periapical region of the teeth or perforation of the oral mucosa can increase risk for IE [23,24].

Some studies have suggested that dental hygiene may be associated with risk of IE [22,25,26]. One study including 73 patients with IE due to oral streptococci and 192 patients with IE due to non-oral pathogens noted that patients with IE due to oral streptococci used toothpicks, dental floss, water jets, and/or an interdental brush more frequently than patients with IE due to non-oral streptococci, but were less likely to brush their teeth after meals; findings on dental examination were similar in both groups [26].

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endothelial damage, predisposing to subsequent infection. Issues related to IE and injection drug use are discussed further separately. (See "Right-sided native valve infective endocarditis".) <span>Poor dentition or dental infection — Poor dentition and/or dental infection are presumed to be risk factors for IE due to oral flora [21,22]. Routine dental cleaning is not a risk factor for IE; dental procedures that involve manipulation of gingival tissue or the periapical region of the teeth or perforation of the oral mucosa can increase risk for IE [23,24]. Some studies have suggested that dental hygiene may be associated with risk of IE [22,25,26]. One study including 73 patients with IE due to oral streptococci and 192 patients with IE due to non-oral pathogens noted that patients with IE due to oral streptococci used toothpicks, dental floss, water jets, and/or an interdental brush more frequently than patients with IE due to non-oral streptococci, but were less likely to brush their teeth after meals; findings on dental examination were similar in both groups [26]. Antimicrobial prophylaxis for prevention of IE is appropriate for patients undergoing invasive dental procedures in the setting of underlying structural heart disease or prosthetic hear




Structural heart disease — Approximately three-fourths of patients with IE have a pre-existing structural cardiac abnormality at the time that endocarditis develops [7,27]. A Danish study including more than 3000 patients with hypertrophic cardiomyopathy, the risk for IE was higher than the population-based controls (hazard ratio [HR] 6.5, 95% CI 2.3-18.5), yet lower than a high-risk population with prosthetic valves (HR 0.13, 95% CI 0.06-0.29) [28]. A Spanish study reported that the proportion of patients without underlying heart conditions increased between 2001 and 2013 (compared with 1987 to 2001) [17]; patients without pre-existing heart disease were more likely to be immunosuppressed and more likely to acquire infection after exposure to health care settings.
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structural heart disease or prosthetic heart valve(s); this is discussed further separately. (See "Antimicrobial prophylaxis for the prevention of bacterial endocarditis".) Comorbid conditions <span>Structural heart disease — Approximately three-fourths of patients with IE have a pre-existing structural cardiac abnormality at the time that endocarditis develops [7,27]. A Danish study including more than 3000 patients with hypertrophic cardiomyopathy, the risk for IE was higher than the population-based controls (hazard ratio [HR] 6.5, 95% CI 2.3-18.5), yet lower than a high-risk population with prosthetic valves (HR 0.13, 95% CI 0.06-0.29) [28]. A Spanish study reported that the proportion of patients without underlying heart conditions increased between 2001 and 2013 (compared with 1987 to 2001) [17]; patients without pre-existing heart disease were more likely to be immunosuppressed and more likely to acquire infection after exposure to health care settings. Antimicrobial prophylaxis for prevention of IE is appropriate for some patients undergoing invasive procedures in the setting of underlying structural heart disease; this is discussed f




Valvular disease — Valvular disease includes rheumatic heart disease, mitral valve prolapse (usually with coexistent mitral regurgitation), aortic valve disease, and other valvular abnormalities.

One report evaluating cases of IE in New York between 1938 and 1967 noted that rheumatic heart disease was a common cardiac abnormality (39 percent of cases) [29]. In contrast, a subsequent series of IE cases between 1980 and 1984 noted the presence of rheumatic heart disease in only 6 percent of patients with IE [27].

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invasive procedures in the setting of underlying structural heart disease; this is discussed further separately. (See "Antimicrobial prophylaxis for the prevention of bacterial endocarditis".) <span>Valvular disease — Valvular disease includes rheumatic heart disease, mitral valve prolapse (usually with coexistent mitral regurgitation), aortic valve disease, and other valvular abnormalities. One report evaluating cases of IE in New York between 1938 and 1967 noted that rheumatic heart disease was a common cardiac abnormality (39 percent of cases) [29]. In contrast, a subsequent series of IE cases between 1980 and 1984 noted the presence of rheumatic heart disease in only 6 percent of patients with IE [27]. Mitral valve disease, such as mitral valve prolapse [30] (usually with coexistent mitral regurgitation) and/or mitral annulus calcification, is a risk factor for IE. Two reports of IE n




Mitral valve disease, such as mitral valve prolapse [30] (usually with coexistent mitral regurgitation) and/or mitral annulus calcification, is a risk factor for IE. Two reports of IE noted mitral valve prolapse was the underlying cardiac lesion in 22 and 29 percent of cases [27,31]. The risk of IE in patients with mitral valve prolapse and associated regurgitation is estimated to be five to eight times higher than that in patients with a normal mitral valve [32,33]. In addition, mitral valve prolapse has been associated with viridans group streptococcal IE [34]. However, mitral valve prolapse without mitral insufficiency is a more common abnormality that is associated with only a small risk of endocarditis.
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ormality (39 percent of cases) [29]. In contrast, a subsequent series of IE cases between 1980 and 1984 noted the presence of rheumatic heart disease in only 6 percent of patients with IE [27]. <span>Mitral valve disease, such as mitral valve prolapse [30] (usually with coexistent mitral regurgitation) and/or mitral annulus calcification, is a risk factor for IE. Two reports of IE noted mitral valve prolapse was the underlying cardiac lesion in 22 and 29 percent of cases [27,31]. The risk of IE in patients with mitral valve prolapse and associated regurgitation is estimated to be five to eight times higher than that in patients with a normal mitral valve [32,33]. In addition, mitral valve prolapse has been associated with viridans group streptococcal IE [34]. However, mitral valve prolapse without mitral insufficiency is a more common abnormality that is associated with only a small risk of endocarditis. Aortic valve disease (sclerosis, stenosis, and/or regurgitation) occurs in 12 to 30 percent of IE cases [35]. (See 'Congenital heart disease' below.) The risk of IE among patients with




Aortic valve disease (sclerosis, stenosis, and/or regurgitation) occurs in 12 to 30 percent of IE cases [35]. (See 'Congenital heart disease' below.)
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ed with viridans group streptococcal IE [34]. However, mitral valve prolapse without mitral insufficiency is a more common abnormality that is associated with only a small risk of endocarditis. <span>Aortic valve disease (sclerosis, stenosis, and/or regurgitation) occurs in 12 to 30 percent of IE cases [35]. (See 'Congenital heart disease' below.) The risk of IE among patients with acquired valvular disorders (ie, aortic stenosis or regurgitation, mitral stenosis or regurgitation, mitral valve prolapse, rheumatic heart disease) c




The risk of IE appears to be low in adults with pulmonary or tricuspid regurgitation due to pulmonary hypertension in the setting of inherently normal pulmonic and tricuspid valves. In one series of 186 such patients who were followed for a mean of nine years, no cases of endocarditis occurred (with the exception of a single intravenous drug abuser) [36].
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atients (HR 0.27, 95% CI 0.23-0.33). The results support our understanding of risk for IE in patients with acquired valve disorders and their categorization as 'moderate' risk for acquiring IE. <span>The risk of IE appears to be low in adults with pulmonary or tricuspid regurgitation due to pulmonary hypertension in the setting of inherently normal pulmonic and tricuspid valves. In one series of 186 such patients who were followed for a mean of nine years, no cases of endocarditis occurred (with the exception of a single intravenous drug abuser) [36]. Congenital heart disease — Congenital heart lesions predisposing to IE include aortic stenosis, bicuspid aortic valve [30], pulmonary stenosis, ventricular septal defect, patent ductus




The risk of IE among patients with acquired valvular disorders (ie, aortic stenosis or regurgitation, mitral stenosis or regurgitation, mitral valve prolapse, rheumatic heart disease) compared with age and sex matched population-based controls was evaluated in a Danish registry between 2000 and 2015 [28]. Patients with a valve disorder had a higher risk of IE compared with matched controls (HR 8.7, 95% CI 6.3-12.0) yet lower risk of IE compared with high-risk prosthetic heart valve patients (HR 0.27, 95% CI 0.23-0.33). The results support our understanding of risk for IE in patients with acquired valve disorders and their categorization as 'moderate' risk for acquiring IE.
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ted with only a small risk of endocarditis. Aortic valve disease (sclerosis, stenosis, and/or regurgitation) occurs in 12 to 30 percent of IE cases [35]. (See 'Congenital heart disease' below.) <span>The risk of IE among patients with acquired valvular disorders (ie, aortic stenosis or regurgitation, mitral stenosis or regurgitation, mitral valve prolapse, rheumatic heart disease) compared with age and sex matched population-based controls was evaluated in a Danish registry between 2000 and 2015 [28]. Patients with a valve disorder had a higher risk of IE compared with matched controls (HR 8.7, 95% CI 6.3-12.0) yet lower risk of IE compared with high-risk prosthetic heart valve patients (HR 0.27, 95% CI 0.23-0.33). The results support our understanding of risk for IE in patients with acquired valve disorders and their categorization as 'moderate' risk for acquiring IE. The risk of IE appears to be low in adults with pulmonary or tricuspid regurgitation due to pulmonary hypertension in the setting of inherently normal pulmonic and tricuspid valves. In




Congenital heart disease — Congenital heart lesions predisposing to IE include aortic stenosis, bicuspid aortic valve [30], pulmonary stenosis, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, and tetralogy of Fallot.

In one series including 2401 patients with congenital aortic stenosis, pulmonary stenosis, or a ventricular septal defect, the incidence of endocarditis was 135 cases/100,000 person-years [37]. IE occurred most frequently among patients with aortic stenosis and ventricular septal defects (271 and 145 cases per 100,000 person-years, respectively). Among patients with aortic stenosis, increasing peak gradient across the aortic valve correlated with increasing risk of IE. In another series, the risk of IE with aortic stenosis was approximately twice as high as with aortic regurgitation (73 versus 40 cases per 100,000 person-years) [38].

Pulmonic stenosis appears to confer a relatively low rate of IE among congenital heart lesions; one case was noted among 592 patients with this lesion [37].

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tricuspid valves. In one series of 186 such patients who were followed for a mean of nine years, no cases of endocarditis occurred (with the exception of a single intravenous drug abuser) [36]. <span>Congenital heart disease — Congenital heart lesions predisposing to IE include aortic stenosis, bicuspid aortic valve [30], pulmonary stenosis, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, and tetralogy of Fallot. In one series including 2401 patients with congenital aortic stenosis, pulmonary stenosis, or a ventricular septal defect, the incidence of endocarditis was 135 cases/100,000 person-years [37]. IE occurred most frequently among patients with aortic stenosis and ventricular septal defects (271 and 145 cases per 100,000 person-years, respectively). Among patients with aortic stenosis, increasing peak gradient across the aortic valve correlated with increasing risk of IE. In another series, the risk of IE with aortic stenosis was approximately twice as high as with aortic regurgitation (73 versus 40 cases per 100,000 person-years) [38]. Pulmonic stenosis appears to confer a relatively low rate of IE among congenital heart lesions; one case was noted among 592 patients with this lesion [37]. Prosthetic heart valve(s) — Issues related to prosthetic heart valves are discussed separately. (See "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis




Prosthetic heart valve(s) — Issues related to prosthetic heart valves are discussed separately. (See "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis".)

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ases per 100,000 person-years) [38]. Pulmonic stenosis appears to confer a relatively low rate of IE among congenital heart lesions; one case was noted among 592 patients with this lesion [37]. <span>Prosthetic heart valve(s) — Issues related to prosthetic heart valves are discussed separately. (See "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis".) Transcatheter aortic valve replacement — The risk for IE among patients with transcatheter aortic valve replacement (TAVR) is believed to be similar to the risk for IE among patients wi




Transcatheter aortic valve replacement — The risk for IE among patients with transcatheter aortic valve replacement (TAVR) is believed to be similar to the risk for IE among patients with surgically placed prosthetic valves [39,40]. Among patients with TAVR, younger age, male gender, diabetes, and moderate to severe aortic regurgitation are associated with higher risk for IE [41].
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37]. Prosthetic heart valve(s) — Issues related to prosthetic heart valves are discussed separately. (See "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis".) <span>Transcatheter aortic valve replacement — The risk for IE among patients with transcatheter aortic valve replacement (TAVR) is believed to be similar to the risk for IE among patients with surgically placed prosthetic valves [39,40]. Among patients with TAVR, younger age, male gender, diabetes, and moderate to severe aortic regurgitation are associated with higher risk for IE [41]. (See "Transcatheter aortic valve implantation: Complications", section on 'Prosthetic valve endocarditis'.) History of infective endocarditis — A prior history of endocarditis is an imp




History of infective endocarditis — A prior history of endocarditis is an important predisposing cause for subsequent IE. In one large cohort of patients who survived IE, recurrent IE occurred in 4.5 percent of patients [42]. Other studies have reported rates of IE recurrence ranging from 2.5 to 9 percent [43].

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moderate to severe aortic regurgitation are associated with higher risk for IE [41]. (See "Transcatheter aortic valve implantation: Complications", section on 'Prosthetic valve endocarditis'.) <span>History of infective endocarditis — A prior history of endocarditis is an important predisposing cause for subsequent IE. In one large cohort of patients who survived IE, recurrent IE occurred in 4.5 percent of patients [42]. Other studies have reported rates of IE recurrence ranging from 2.5 to 9 percent [43]. Intravascular device — Bacteremia associated with the presence of an intravenous catheter or an invasive intravascular procedure can be complicated by health care-associated endocarditi




Intravascular device — Bacteremia associated with the presence of an intravenous catheter or an invasive intravascular procedure can be complicated by health care-associated endocarditis [6,44-48]. Among 2781 patients with IE in one cohort, 23 percent of cases were health care associated [49,50]. Less common intravascular devices with risk for IE include peritoneovenous shunts for the control of intractable ascites [51] and ventriculoatrial shunts for the management of hydrocephalus [52].
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E. In one large cohort of patients who survived IE, recurrent IE occurred in 4.5 percent of patients [42]. Other studies have reported rates of IE recurrence ranging from 2.5 to 9 percent [43]. <span>Intravascular device — Bacteremia associated with the presence of an intravenous catheter or an invasive intravascular procedure can be complicated by health care-associated endocarditis [6,44-48]. Among 2781 patients with IE in one cohort, 23 percent of cases were health care associated [49,50]. Less common intravascular devices with risk for IE include peritoneovenous shunts for the control of intractable ascites [51] and ventriculoatrial shunts for the management of hydrocephalus [52]. Nosocomial endocarditis has been defined as a diagnosis of IE made more than 72 hours after admission in patients with no evidence of IE on admission or IE that develops within 60 days




Nosocomial endocarditis has been defined as a diagnosis of IE made more than 72 hours after admission in patients with no evidence of IE on admission or IE that develops within 60 days of a previous hospital admission during which there was risk for bacteremia or IE [44]. In one report from Minnesota, health care-associated IE accounted for 50 percent of all IE cases during the period 2001 to 2006; of these, 7.5 percent were nosocomial and 42.5 percent were community acquired [8].

Nosocomial endocarditis may be due to unusual pathogens; for example, endocarditis due to nontuberculous mycobacteria has occurred following open-chest heart surgery in patients from several European countries [53].

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ss common intravascular devices with risk for IE include peritoneovenous shunts for the control of intractable ascites [51] and ventriculoatrial shunts for the management of hydrocephalus [52]. <span>Nosocomial endocarditis has been defined as a diagnosis of IE made more than 72 hours after admission in patients with no evidence of IE on admission or IE that develops within 60 days of a previous hospital admission during which there was risk for bacteremia or IE [44]. In one report from Minnesota, health care-associated IE accounted for 50 percent of all IE cases during the period 2001 to 2006; of these, 7.5 percent were nosocomial and 42.5 percent were community acquired [8]. Nosocomial endocarditis may be due to unusual pathogens; for example, endocarditis due to nontuberculous mycobacteria has occurred following open-chest heart surgery in patients from several European countries [53]. Cardiac implantable electronic device — Infection of a cardiac implantable electronic device (CIED) is a risk factor for IE [28]. CIED-related IE can manifest as lead vegetation and/or




Cardiac implantable electronic device — Infection of a cardiac implantable electronic device (CIED) is a risk factor for IE [28]. CIED-related IE can manifest as lead vegetation and/or valve vegetation.
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s may be due to unusual pathogens; for example, endocarditis due to nontuberculous mycobacteria has occurred following open-chest heart surgery in patients from several European countries [53]. <span>Cardiac implantable electronic device — Infection of a cardiac implantable electronic device (CIED) is a risk factor for IE [28]. CIED-related IE can manifest as lead vegetation and/or valve vegetation. (See "Infections involving cardiac implantable electronic devices: Epidemiology, microbiology, clinical manifestations, and diagnosis".) Chronic hemodialysis — Chronic hemodialysis pati




Chronic hemodialysis — Chronic hemodialysis patients are at significant risk for IE [54,55]. Predisposing factors include intravascular access, calcific valvular disease, and immune impairment [55]. The incidence of IE in hemodialysis patients has been estimated to be 308 per 100,000 patient-years [54-56]. However, the accuracy of such estimates is difficult to assess given potential bias related to variable use of echocardiography for evaluation of access-related bloodstream infections, the infrequency of postmortem exams in hemodialysis patients following bacteremia, inconsistent follow-up, and the retrospective design of most studies.
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can manifest as lead vegetation and/or valve vegetation. (See "Infections involving cardiac implantable electronic devices: Epidemiology, microbiology, clinical manifestations, and diagnosis".) <span>Chronic hemodialysis — Chronic hemodialysis patients are at significant risk for IE [54,55]. Predisposing factors include intravascular access, calcific valvular disease, and immune impairment [55]. The incidence of IE in hemodialysis patients has been estimated to be 308 per 100,000 patient-years [54-56]. However, the accuracy of such estimates is difficult to assess given potential bias related to variable use of echocardiography for evaluation of access-related bloodstream infections, the infrequency of postmortem exams in hemodialysis patients following bacteremia, inconsistent follow-up, and the retrospective design of most studies. HIV infection — It has been suggested that HIV infection is an independent risk factor for IE in injection drug abusers [57]; however, this has not been confirmed in other reports [58].




HIV infection — It has been suggested that HIV infection is an independent risk factor for IE in injection drug abusers [57]; however, this has not been confirmed in other reports [58]. Unusual organisms such as Salmonella and Listeria may cause IE in HIV-infected patients [58,59].
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f access-related bloodstream infections, the infrequency of postmortem exams in hemodialysis patients following bacteremia, inconsistent follow-up, and the retrospective design of most studies. <span>HIV infection — It has been suggested that HIV infection is an independent risk factor for IE in injection drug abusers [57]; however, this has not been confirmed in other reports [58]. Unusual organisms such as Salmonella and Listeria may cause IE in HIV-infected patients [58,59]. MICROBIOLOGY — A variety of microorganisms can cause infective endocarditis (IE), and the microbiology of IE can vary depending on the population. The microbiology of IE in patients who




The three most common causes of IE worldwide are staphylococci, streptococci, and enterococci. In the United States and most developed countries, Staphylococcus aureus is the most common cause of IE; while streptococci has been shown to be the most common cause in some older, population-based studies [4,8]. Staphylococcal IE is a common cause of health care-associated IE [49]; streptococcal IE is a common cause of community-acquired IE [13].
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rosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis", section on 'Microbiology' and "Right-sided native valve infective endocarditis", section on 'Microbiology'.) <span>The three most common causes of IE worldwide are staphylococci, streptococci, and enterococci. In the United States and most developed countries, Staphylococcus aureus is the most common cause of IE; while streptococci has been shown to be the most common cause in some older, population-based studies [4,8]. Staphylococcal IE is a common cause of health care-associated IE [49]; streptococcal IE is a common cause of community-acquired IE [13]. Among 2781 patients with IE in a large cohort, the distribution of pathogens was as follows [50,60,61]: ●S. aureus – 31 percent ●Viridans group streptococci – 17 percent ●Enterococci –




Among 2781 patients with IE in a large cohort, the distribution of pathogens was as follows [50,60,61]:

S. aureus – 31 percent

● Viridans group streptococci – 17 percent

● Enterococci – 11 percent

● Coagulase-negative staphylococci – 11 percent

Streptococcus bovis – 7 percent

● Other streptococci (including nutritionally variant streptococci) – 5 percent

● Non-HACEK gram-negative bacteria – 2 percent

● Fungi – 2 percent

● HACEK – 2 percent; organisms in this category include a number of fastidious gram-negative bacilli: Haemophilus aphrophilus (subsequently called Aggregatibacter aphrophilus and Aggregatibacter paraphrophilus); Actinobacillus actinomycetemcomitans (subsequently called Aggregatibacter actinomycetemcomitans); Cardiobacterium hominis; Eikenella corrodens; and Kingella kingae

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mon cause in some older, population-based studies [4,8]. Staphylococcal IE is a common cause of health care-associated IE [49]; streptococcal IE is a common cause of community-acquired IE [13]. <span>Among 2781 patients with IE in a large cohort, the distribution of pathogens was as follows [50,60,61]: ●S. aureus – 31 percent ●Viridans group streptococci – 17 percent ●Enterococci – 11 percent ●Coagulase-negative staphylococci – 11 percent ●Streptococcus bovis – 7 percent ●Other streptococci (including nutritionally variant streptococci) – 5 percent ●Non-HACEK gram-negative bacteria – 2 percent ●Fungi – 2 percent ●HACEK – 2 percent; organisms in this category include a number of fastidious gram-negative bacilli: Haemophilus aphrophilus (subsequently called Aggregatibacter aphrophilus and Aggregatibacter paraphrophilus); Actinobacillus actinomycetemcomitans (subsequently called Aggregatibacter actinomycetemcomitans); Cardiobacterium hominis; Eikenella corrodens; and Kingella kingae The remaining cases included culture-negative endocarditis (8 percent), polymicrobial (1 percent), and a variety of other organisms (3 percent). The higher incidence of S. aureus relati




The higher incidence of S. aureus relative to viridans group streptococci is likely because this study was conducted in large, tertiary care centers and may not reflect the epidemiology of IE in more rural communities.
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ominis; Eikenella corrodens; and Kingella kingae The remaining cases included culture-negative endocarditis (8 percent), polymicrobial (1 percent), and a variety of other organisms (3 percent). <span>The higher incidence of S. aureus relative to viridans group streptococci is likely because this study was conducted in large, tertiary care centers and may not reflect the epidemiology of IE in more rural communities. In the setting of streptococcal bacteremia, species differentiation can be useful to determine the likelihood of IE. As an example, in a study including more than 6000 streptococcal blo




In the setting of streptococcal bacteremia, species differentiation can be useful to determine the likelihood of IE. As an example, in a study including more than 6000 streptococcal bloodstream infections, using Streptococcus pneumoniae as a reference, the risk of IE with Streptococcus mutans (odds ratio [OR] 81.3 [37.6-176]), Streptococcus gordonii (OR 80.8 [43.9-149]), and Streptococcus sanguinis (OR 59.1 [32.6-107]) bacteremia (among others) was high, while the risk for IE with Streptococcus pyogenes bacteremia (OR 1.57 [0.78-3.18]) was comparatively low [62]. Differential risk for IE among streptococcal bloodstream isolates has been shown in other studies, as well [63,64].
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. aureus relative to viridans group streptococci is likely because this study was conducted in large, tertiary care centers and may not reflect the epidemiology of IE in more rural communities. <span>In the setting of streptococcal bacteremia, species differentiation can be useful to determine the likelihood of IE. As an example, in a study including more than 6000 streptococcal bloodstream infections, using Streptococcus pneumoniae as a reference, the risk of IE with Streptococcus mutans (odds ratio [OR] 81.3 [37.6-176]), Streptococcus gordonii (OR 80.8 [43.9-149]), and Streptococcus sanguinis (OR 59.1 [32.6-107]) bacteremia (among others) was high, while the risk for IE with Streptococcus pyogenes bacteremia (OR 1.57 [0.78-3.18]) was comparatively low [62]. Differential risk for IE among streptococcal bloodstream isolates has been shown in other studies, as well [63,64]. Nutritionally variant streptococci, Abiotrophia spp and Granulicatella spp, account for a small proportion of streptococcal IE cases. The clinical presentation of IE due to these pathog




Nutritionally variant streptococci, Abiotrophia spp and Granulicatella spp, account for a small proportion of streptococcal IE cases. The clinical presentation of IE due to these pathogens is similar to that of viridans group streptococci. Diminished susceptibility to penicillins and cephalosporins in these species has been described [60,61].
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ococcus pyogenes bacteremia (OR 1.57 [0.78-3.18]) was comparatively low [62]. Differential risk for IE among streptococcal bloodstream isolates has been shown in other studies, as well [63,64]. <span>Nutritionally variant streptococci, Abiotrophia spp and Granulicatella spp, account for a small proportion of streptococcal IE cases. The clinical presentation of IE due to these pathogens is similar to that of viridans group streptococci. Diminished susceptibility to penicillins and cephalosporins in these species has been described [60,61]. Between 2000 and 2011, the incidence of streptococcal IE in the United States increased significantly, from 26 to 42 cases per million population [2]; it is uncertain whether this obser




Between 2000 and 2011, the incidence of streptococcal IE in the United States increased significantly, from 26 to 42 cases per million population [2]; it is uncertain whether this observation is a reflection of changes to guidelines regarding antimicrobial prophylaxis for prevention of IE published in 2007.
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entation of IE due to these pathogens is similar to that of viridans group streptococci. Diminished susceptibility to penicillins and cephalosporins in these species has been described [60,61]. <span>Between 2000 and 2011, the incidence of streptococcal IE in the United States increased significantly, from 26 to 42 cases per million population [2]; it is uncertain whether this observation is a reflection of changes to guidelines regarding antimicrobial prophylaxis for prevention of IE published in 2007. (See "Antimicrobial prophylaxis for the prevention of bacterial endocarditis".) Gram-negative bacteria such as Escherichia coli and Klebsiella pneumoniae adhere less readily to heart va




Gram-negative bacteria such as Escherichia coli and Klebsiella pneumoniae adhere less readily to heart valves than gram-positive organisms [65].
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a reflection of changes to guidelines regarding antimicrobial prophylaxis for prevention of IE published in 2007. (See "Antimicrobial prophylaxis for the prevention of bacterial endocarditis".) <span>Gram-negative bacteria such as Escherichia coli and Klebsiella pneumoniae adhere less readily to heart valves than gram-positive organisms [65]. Brucella is an important cause of IE in regions where it is endemic [66]. (See "Brucellosis: Treatment and prevention", section on 'Endocarditis'.) Patients with ulcerative lesions of t




Brucella is an important cause of IE in regions where it is endemic [66].
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for the prevention of bacterial endocarditis".) Gram-negative bacteria such as Escherichia coli and Klebsiella pneumoniae adhere less readily to heart valves than gram-positive organisms [65]. <span>Brucella is an important cause of IE in regions where it is endemic [66]. (See "Brucellosis: Treatment and prevention", section on 'Endocarditis'.) Patients with ulcerative lesions of the colon due to carcinoma or inflammatory bowel disease have a predilectio




Patients with ulcerative lesions of the colon due to carcinoma or inflammatory bowel disease have a predilection to develop IE due to S. bovis [67,68]
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art valves than gram-positive organisms [65]. Brucella is an important cause of IE in regions where it is endemic [66]. (See "Brucellosis: Treatment and prevention", section on 'Endocarditis'.) <span>Patients with ulcerative lesions of the colon due to carcinoma or inflammatory bowel disease have a predilection to develop IE due to S. bovis [67,68]. (See "Infections due to group D streptococci (Streptococcus bovis/Streptococcus equinus complex)", section on 'Association with colonic neoplasia'.) Fungal IE is rare. Candida spp [69-




Fungal IE is rare. Candida spp [69-71] and Aspergillus spp [72,73] are the major causes of fungal IE
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ction to develop IE due to S. bovis [67,68]. (See "Infections due to group D streptococci (Streptococcus bovis/Streptococcus equinus complex)", section on 'Association with colonic neoplasia'.) <span>Fungal IE is rare. Candida spp [69-71] and Aspergillus spp [72,73] are the major causes of fungal IE. (See "Candida endocarditis and suppurative thrombophlebitis" and "Epidemiology and clinical manifestations of invasive aspergillosis", section on 'Endocarditis'.) Interpretation of cul




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L'incidence de l'endocardite infectieuse est estimée autour de 30 cas par million d'habitants et par an dans les études en population générale conduites dans les pays occidentaux
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Une enquête épidémiologique a été menée en France en 1991, 1999 et 2008 selon la même méthodologie. Un des avantages de ces enquêtes était de comporter une validation de chaque cas utilisant la classification de Duke à partir des dossiers médicaux. L'enquête effectuée en 2008 concernait 32 % de la population française adulte et rapportait une incidence de 34 cas d'endo- cardites par million d'habitants et par an, classées comme certaines selon la classification de Duke [1].
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L'enquête effectuée en 2008 concernait 32 % de la population française adulte et rapportait une incidence de 34 cas d'endo- cardites par million d'habitants et par an, classées comme certaines selon la classification de Duke [1]. Il existait une nette prédominance masculine (incidence annuelle de 51 cas par million chez les hommes vs 16 chez les femmes). Chez les hommes, l'incidence annuelle était < 30 cas par million avant l'âge de 50 ans et augmentait à près de 200 cas par million entre 75 et 79 ans [1].
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D'autres études ont été menées en Australie, en Italie et aux États-Unis sur des bases régionales et ont rapporté une inci- dence annuelle entre 40 et 80 cas d'endocardite par million d'habitants (tableau I) [2–4].
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Des données plus récentes pro- viennent de registres nationaux conduits en Angleterre et au Danemark et sont basées sur les codes diagnostiques hospita- liers [5–7]. Dans l'étude anglaise, les données étaient concor- dantes avec l'enquête nationale française, l'incidence annuelle de l'endocardite infectieuse étant estimée à 36 cas par million d'habitants [5].
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[unknown IMAGE 6284694392076]
Endocardite infectieuse épidémiologie
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La mortalité précoce demeure élevée, entre 15 et 25 % durant la période hospitalière ou les 3 premiers mois [1–4]
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Le staphylocoque est le micro-organisme désormais le plus souvent à l'origine de l'endocardite infectieuse, suivi par les streptocoques d'origine bucco-dentaire, puis l'entérocoque.
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De façon concordante, la porte d'entrée la plus fréquente est cutanée, suivie par les portes d'entrée bucco-dentaires et digestives [8].
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La fréquence des endocardites à hémocultures négatives est devenue faible, entre 5 et 10 %, en raison des progrès des techniques d'identification microbiologique et du recours aux sérologies.
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La prédominance du staphylocoque est le plus souvent rappor- tée à l'augmentation de fréquence des endocardites liées aux soins. Ceci regroupe les endocardites nosocomiales (acquises en milieu hospitalier) et nosohusiales (acquises lors de procédures de soins en dehors du milieu hospitalier). L'ensemble des endocardites liées aux soins représente 30 à 50 % de l'ensemble des endocardites et 40 à 50 % sont dues au staphylocoque doré (tableau I). Leur mortalité intrahospitalière est plus élevée que celle des endocardites acquises en milieu communautaire [4].
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Les endocardites postopératoires sont définies par leur survenue durant la première année suivant une chirurgie valvulaire. Leur profil microbiologique est caractérisé par la prédominance du staphylocoque doré et du staphylocoque à coagulase négative alors que les streptocoques sont rares. Après la première année, la répartition des micro-organismes des endocardites sur pro- thèses implantées chirurgicalement est voisine de celle des endocardites sur valve native
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La répartition des micro-organis- mes est différente dans les endocardites après implantation de prothèse par cathéter (TAVI), notamment en raison d'une fré- quence accrue d'Enterococcus faecalis [9]. Ces différences ne semblent pas imputables au type de prothèse ou à son mode d'implantation, mais surtout à la population étudiée. En effet, E. faecalis est plus souvent responsable d'endocardite chez le sujet âgé, y compris sur valve native, avec une fréquence de 22 % chez les patients de plus de 80 ans, ce qui représente une fréquence deux fois plus élevée que chez les patients âgés de moins de 65 ans [10]
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Dans les études en population générale, 13 à 21 % des endo- cardites surviennent sur des prothèses valvulaires, environ 13 % sur des dispositifs de stimulation et 6 à 7 % chez les patients ayant des antécédents d'endocardite [1–4].
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En présence d'une valvulopathie native, l'incidence est de l'ordre de 1 à 3 pour 1000 ; en présence d'une prothèse valvulaire ou d'une chirurgie valvulaire conservatrice avec implantation de matériel prothétique, l'incidence est plus élevée, entre 4 et 6 pour 1000 [5–7].
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Dans une étude sur la base de donnée nationale danoise, l'incidence de l'endocardite était plus élevée en pré- sence d'une bioprothèse que d'une prothèse mécanique, y compris après ajustement pour les facteurs de confusion [11]
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L'incidence de l'endocardite après TAVI est estimée entre 11 et 16 pour 1000 [9].
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L'incidence annuelle de l'endocardite sur matériel de stimula- tion est estimée entre 0,5 et 2 pour 1000, elle augmente avec le nombre de sondes de stimulation et en présence d'un défibril- lateur [5,7]
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L'incidence de l'endocardite infectieuse est particulièrement élevée, entre 10 et 15 pour 1000 chez les patients qui ont déjà présenté un épisode d'endocardite [5,6].
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Dans les enquêtes épidémiologiques françaises, l'incidence standar- disée de l'endocardite ne différait pas entre les trois enquêtes conduites en 1991, 1999 et 2008 [15]. Une augmentation de l'incidence de l'endocardite a été rapportée notamment d'après les données du Royaume-Uni entre 2000 et 2013
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[unknown IMAGE 6284721655052]
FDR endocardite infectieuse
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La relation temporelle avec la modi- fication des recommandations d'antibioprophylaxie n'a été étu- diée spécifiquement que dans l'étude britannique, mais son interprétation a fait l'objet de critiques méthodologiques
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Il n'existe pas de grande série permettant d'estimer l'incidence de l'endocardite dans les pays en voie de développement. Sur le plan qualitatif, la présentation est très différente de celle des pays occidentaux [26]. Les patients sont nettement plus jeunes, ce qui correspond à la persistance de l'endémie rhumatismale, qui est à l'origine de valvulopathies sévères chez les adultes jeunes. Le streptocoque demeure le micro-organisme le plus souvent responsable et les endocardites à hémocultures néga- tives sont plus fréquentes. Selon les estimations du Global Burden Disease, l'endocardite était responsable de 65 000 décès dans le monde en 2013 [27]
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L'endothélium valvulaire normal est résistant à infection, mais son altération en raison d'une valvulopathie native expose les composants de la matrice extracellulaire du sous-endothélium qui sont thrombogènes et déclenchent une adhésion et une activation des plaquettes, suivie d'une colonisation rapide par les micro-organismes circu- lants, qui infectent ensuite les cellules endothéliales
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Il existe des différences d'affinité des micro-organismes pour l'endothé- lium valvulaire et le thrombus qui dépendent de molécules d'adhésion (MSCRAMM : microbial surface component reacting with adhesive matrix molecules)
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[unknown IMAGE 6284732140812]
Incidence Endocardite infectieuse
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Des protéines se liant au fibrinogène ou à la fibronectine sont présentes à la surface des micro-organismes. Certains micro-organismes comme le staphylocoque doré peuvent également se lier directement aux cellules endothéliales.
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Les propriétés de ces nombreuses molécules d'adhésion expliquent la prédominance des cocci gram positifs comme micro-organismes responsables
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L'adhésion des micro-organismes est également favorisée par l'expression des intégrines par les cellules endothéliales en réponse à l'inflammation
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Après la face d'adhésion, les micro- organismes peuvent être internalisés par les cellules endothé- liales où ils peuvent proliférer et diffuser ou persister en échap- pant aux antibiotiques et au système immunitaire. Les mécanismes de colonisation de l'endothélium valvulaire diffèrent et sont mal connus en ce qui concerne les micro- organismes à développement intracellulaire exclusif, comme Coxiella burnetii et Bartonella
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Certains micro-organismes, en particulier le staphylocoque doré, accompagnent leur prolifération de la formation d'un biofilm conduisant à un agrégat plaquettaire enchâssé dans un réseau de polysaccharides et de protéines. La formation d'un biofilm favorise la virulence de l'infection, notamment en protégeant les micro-organismes des défenses immunitaires et des traite- ments antimicrobiens. Le biofilm semble jouer un rôle particu- lièrement important dans les endocardites sur prothèse et sur matériel de stimulation, alors que son rôle n'est pas prouvé dans les endocardites sur valves natives [28]
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La colonisation du thrombus fibrino-plaquettaire par les micro-organismes circulants déclenche une réaction immuni- taire activant les monocytes circulants qui sécrètent du facteur tissulaire et des cytokines.
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les mutilations valvulaires (perforations ou déchirures) et péri- valvulaires (abcès) sont les conséquences de la destruction de la matrice extracellulaire par les enzymes protéolytiques libé- rés par les micro-organismes et les cellules inflammatoires ; l'activation du système immunitaire entraîne la formation de complexes immuns circulants qui peuvent entraîner ensuite des lésions auto-immunes comme la glomérulonéphrite, les taches de Roth au fond d'œil et les nodosités d'Osler. La présence du facteur rhumatoïde est un critère mineur de la classification de Duke. Des anticorps dirigés contre le cyto- plasme des polynucléaires neutrophiles (ANCA) sont détectés dans l'endocardite infectieuse chez près d'un quart des patients
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Des modèles animaux expérimentaux ont montré que l'endo- cardite peut survenir à l'issue de bactériémies brèves avec un inoculum important, mais aussi de bactériémies répétées ou persistantes avec un inoculum faible. Ces bactériémies répétées de faible intensité correspondent à des situations de la vie quotidienne aussi banales que le brossage des dents et la mastication et sont favorisées par une mauvaise hygiène bucco-dentaire
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Les endocardites postopératoires sur prothèse valvulaire sont généralement liées à une contamination péri-opératoire. De même, les endocardites sur matériel de stimulation sont le plus souvent secondaires à une contamination cutanée durant l'implantation ou le remplacement du matériel
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L'examen anatomo-pathologique est plus sensible que la culture de valve pour le diagnostic d'endocardite infectieuse.
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Les végétations sont des thrombi septiques, qui sont le plus souvent implantés sur le versant d'amont des feuillets valvu- laires ou des shunts, ce qui correspond aux zones de basse pression où les conditions rhéologiques favorisent l'agrégation plaquettaire sur le tissu valvulaire pathologique ou sur un matériel étranger (figure 2)
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Il existe un continuum entre la taille de la végétation et le risque embolique
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Lorsque les embolies sont dépistées par des examens très sensibles, comme l'imagerie par résonance magnétique, le risque embolique augmente dès que la longueur de la végéta- tion dépasse 4 mm [30].
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#EpidemiologieEndocardite #Maladies-infectieuses-et-tropicales #Metabolomics #Projet #Thèse
Le risque embolique décroît rapidement après l'instauration du traitement antibiotique
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#EpidemiologieEndocardite #Maladies-infectieuses-et-tropicales #Metabolomics #Projet #Thèse
Les lésions des valves natives débutent par des abcédations fragilisant le tissu valvulaire, qui évoluent vers des déchirures ou des perforations à l'origine de régurgitations valvulaires (figure 3)
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#EpidemiologieEndocardite #Maladies-infectieuses-et-tropicales #Metabolomics #Projet #Thèse
La diffusion de l'infection à la périphérie des valves cause des abcès péri-valvulaires qui consistent initialement en un épaississement qui évolue rapidement vers la détersion et la formation de néocavités.
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La formation d'abcès péri-valvulaires est favorisée par la virulence des micro-organismes, comme le staphylocoque doré, ainsi que par la présence de matériel étranger et sont donc plus fréquentes dans les endocardites sur prothèse que dans les endocardites sur valve native. Les abcès péri-valvulaires sont plus fréquents dans les localisations aortiques que mitrales
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Les régurgitations valvulaires ou péri-valvulaires compliquant une endocardite infectieuse ont la particularité d'apparaître rapidement, ce qui les différencie des autres causes de valvu- lopathies qui sont le plus souvent à l'origine de régurgitations chroniques
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Les lésions vasculaires les plus fréquentes sont les embolies consécutives à la migration des végétations ou de leurs frag- ments.
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La prévalence des anévrysmes mycotiques est estimée entre 1 et 10 %, probablement sous-estimée en l'absence de dépistage systématique
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Flashcard 6286879100172

Question
1. Вектор перемещения по определению:
Answer
[default - edit me]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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Flashcard 6286880148748

Question
[default - edit me]
Answer
∆~r = ~r − ~r 0

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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Flashcard 6286881197324

Question
Средняя скорость: h~v i = ~v + ~v 0 2 ,
Answer
[default - edit me]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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