| Infective endocarditis | |
|---|---|
| Other names | Bacterial endocarditis |
 | |
| Amitral valvevegetation caused by bacterial endocarditis | |
| Specialty | Cardiology,infectious disease |
| Symptoms | Fever,small areas of bleeding into the skin,heart murmur, feeling tired,low red blood cells[1] |
| Complications | Valvular insufficiency,heart failure,stroke,kidney failure[1][2] Blood clot in a lung artery (pulmonary embolism)[3] Enlarged and painful spleen, kidney damage, damage to the distal extremities such as fingers and toes.[4] |
| Causes | Bacterial infection,fungal infection[1] |
| Risk factors | Valvular heart disease includingrheumatic disease,congenital heart disease,[5]artificial valves,hemodialysis,intravenous drug use,electronic pacemakers[6][7] |
| Diagnostic method | Based on symptoms,blood cultures,ultrasound[1] |
| Treatment | Antibiotics,heart surgery[1] |
| Prognosis | 25% risk of death[6] |
| Frequency | 5 per 100,000 per year[6] |
Infective endocarditis is aninfection of the inner surface of the heart (endocardium), usually thevalves.[1]Signs and symptoms may includefever,small areas of bleeding into the skin,heart murmur, feeling tired, andlow red blood cell count.[1][8] Complications may includebackward blood flow in the heart,heart failure – the heart struggling to pump a sufficient amount of blood to meet the body's needs,abnormal electrical conduction in the heart,stroke, andkidney failure.[1][2][8][9]
The cause is typically abacterial infection and less commonly afungal infection.[1] Risk factors includevalvular heart disease, includingrheumatic disease,congenital heart disease,artificial valves,hemodialysis,intravenous drug use, andelectronic pacemakers.[6][7][5] The bacteria most commonly involved arestreptococci orstaphylococci.[1] Diagnosis is suspected based on symptoms and supported byblood cultures orultrasound of the heart.[1] There is also anoninfective form ofendocarditis.[1]
The usefulness ofantibiotics followingdental procedures for prevention is unclear.[10] Some recommend them for people at high risk.[1] Treatment is generally withintravenous antibiotics.[1] The choice of antibiotics is based on the results of blood cultures.[1] Occasionallyheart surgery is required.[1]The number of people affected is about 5 per 100,000 per year.[6] Rates, however, vary between regions of the world.[6] Infective endocarditis occurs in males more often than in females.[1] The risk of death among those infected is about 25%.[6] Without treatment, it is almost universally fatal.[1] Improved diagnosis and treatment options have significantly enhanced the life expectancy of patients with infective endocarditis, particularly with congenital heart disease.[5]
Infective endocarditis is divided into three categories of acute, subacute, and chronic based on the duration of symptoms.[11] Acute infective endocarditis refers to the presence of signs and symptoms of infective endocarditis that are present for days up to six weeks.[11] If these signs and symptoms persist for more than six weeks but less than three months, this is subacute infective endocarditis.[11] Chronic infective endocarditis refers to the presence of such signs and symptoms when they persist for more than three months.[11]
This classification is now discouraged because the ascribed associations (in terms of organism and prognosis) were not strong enough to be relied upon clinically. The termsshort incubation (meaning less than about six weeks) andlong incubation (greater than about six weeks) are preferred.[13]
Infective endocarditis may also be classified asculture-positive orculture-negative. By far the most common cause of "culture-negative" endocarditis is prior administration of antibiotics and can occur in up to 31% of cases.[14][7]
Sometimesmicroorganisms can take a longer period to grow in the culture media, for example Cutibacterium spp.[15] and the HACEK bacteria group. Some organisms are said to befastidious because they have demanding growth requirements. Some examples include pathogens likeAspergillus species,Brucella species,Coxiella burnetii,Chlamydia species. Due to delay in growth and identification in these cases, patients may be erroneously classified as "culture-negative" endocarditis.[16]
Endocarditis can also be classified by the side of the heart affected:
Another form of endocarditis ishealthcare-associated endocarditis when the infecting organism is believed to be transmitted in a health care setting like a hospital, dialysis unit, or a residential nursing home.Nosocomial endocarditis is a form of healthcare associated endocarditis in which the infective organism is acquired during a stay in a hospital and it is usually secondary to presence of intravenous catheters,total parenteral nutrition lines,pacemakers, etc.[17]
Finally, the distinction betweennative-valve endocarditis andprosthetic-valve endocarditis is clinically important. Prosthetic valve endocarditis can be early (within 1 year of surgery) or late (> 1 year following valvular surgery).[7]
Prosthetic valve endocarditis is commonly caused byStaphylococcus epidermidis as it is capable of growing as abiofilm on plastic surfaces.[18]Cutibacterium acnes almost exclusively causes endocarditis on prosthetic heart valves.[15]
Many microorganisms can cause infective endocarditis. These are generally isolated byblood culture, where the patient's blood is drawn and any growth is noted and identified. The term bacterial endocarditis (BE) is commonly used, reflecting the fact that most cases of IE are due to bacteria; however, infective endocarditis (IE) has become the preferred term.[7]
Staphylococcus aureus is the leading cause of infective endocarditis in most parts of the world and is responsible for about 31% of cases.[11] Staphylococcus aureus is the most common cause of endocarditis in people who use intravenous drugs.[23]Viridans streptococci andEnterococci are the second and third most common organisms responsible for infective endocarditis.[11] Viridans streptococci are a common cause of infective endocarditis in South America. OtherStreptococci are also a frequent cause. Infective endocarditis due toStreptococcus bovis occurs more commonly in Europe than in North America.[11] Infection with theHACEK group of bacteria is also a rare cause of infective endocarditis in North America.[24]
The viridans group includesS. oralis,S. mitis,S. sanguis,S. gordonii, andS. parasanguis. The primary habitats for these organisms are the oral cavity and the upper respiratory tract.[25] These bacteria are present in the normal oral flora and enter the bloodstream due to disruption of tissues in the mouth when dental surgical procedures are performed (tooth extractions) or genitourinary manipulation. Similarly, HACEK organisms are a group of bacteria that live on the dental gums and can be seen in people who inject drugs who contaminate their needles with saliva. Patients may also have a history of poor dental hygiene or pre-existing valvular disease.[26]
Viridansalpha-hemolyticstreptococci, which are present in the mouth, are the most frequently isolated microorganisms when the infection is acquired in a community setting. In contrast,Staphylococcus bloodstream infections are frequently acquired in a health care setting where they can enter the bloodstream through procedures that cause breaks in the integrity of skin, such as surgery, catheterization, or during access of long term indwelling catheters or secondary to intravenous injection of recreational drugs.[citation needed]
Enterococcus can enter the bloodstream as a consequence of abnormalities in the gastrointestinal or genitourinary tracts.[citation needed]
Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.
Multiple case reports of infective endocarditis caused by unusual organisms have been published.Cutibacterium spp., which are normal skin flora, have been responsible for infective endocarditis, preferably in patients with prosthetic heart valves, in rare cases leading to death.[31]Tropheryma whipplei has caused endocarditis without gastrointestinal involvement.[32]Citrobacter koseri was found in an immunocompetent adult.[33]Neisseria bacilliformis was found in a person with abicuspid aortic valve.[34]
One in eight cases of infective endocarditis is thought to be caused by viridans streptococci infection associated with dental procedures such as cleaning or toothextraction[25][obsolete source]. This was thought to be more clinically significant than it is[citation needed]. However, it is important that a dentist or a dental hygienist be told of any heart problems before commencing treatment. Prophylacticantibiotics were regularly administered to patients with certain heart conditions as a precaution, although this practice has changed in the US, with new American Heart Associationguidelines released in 2007,[35] and in the UK as of March 2008 due to newNICE guidelines.
Fungal endocarditis (FE) is often fatal and one of the most serious forms of infective endocarditis. The types of fungi most seen associated with this disease are:
Candida albicans is found as a spherical or oval buddingyeast. It is associated with endocarditis in people who inject drugs, patients withprosthetic valves, andimmunocompromised patients. It forms biofilms around thick-walled resting structures like prosthetic heart valves and additionally colonizes and penetratesendothelial walls.[25] C. albicans is responsible for 24-46% of all the cases of FE, and itsmortality rate is 46.6–50%.[36]
Other fungi demonstrated to cause endocarditis areHistoplasma capsulatum andAspergillus.[30] Aspergillus contributes to roughly 25% of FE cases.[36] Endocarditis withTricosporon asahii has also been reported in a case report.[37]
Risk factors for infective endocarditis are based on the premise that in a healthy individual,bacteremia (bacteria entering the bloodstream) is cleared quickly with no adverse consequences.[38] However, if a heart valve is damaged, the bacteria can attach themselves to the valve, resulting in infective endocarditis. Additionally, in individuals with weakened immune systems, the concentration of bacteria in the blood can reach levels high enough to increase the probability that some will attach to the valve. Some significant risk factors are listed here:[11][38]
Damaged valves andendocardium contribute to the development of infective endocarditis.[38] Specifically, the damaged part of aheart valve forms a localblood clot, a condition known asnon-bacterial thrombotic endocarditis (NBTE). The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and formvegetations. As previously mentioned, the body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis.[citation needed]
Damage to the valves and endocardium can be caused by:[38]
Therisk factors for infective endocarditis provide a more extensive list of conditions that can damage the heart.
In general, the Duke criteria should be fulfilled in order to establish the diagnosis of endocarditis.[11][39] Although the Duke criteria are widely used, they have significant limitations.[11] For example, the sensitivity of the Duke criteria for detecting infective endocarditis decreases when prosthetic heart valves are present.[11]
As the Duke criteria rely heavily on the results of echocardiography, research has addressed when to order anechocardiogram by using signs and symptoms to predict occult endocarditis among people who inject drugs[40][41][42] and among non drug-abusing patients.[43][44] However, this research is over twenty years old and it is possible that changes in the epidemiology of endocarditis and bacteria such asstaphylococci make the following estimates incorrect.
The blood testsC reactive protein (CRP) andprocalcitonin have not been found to be particularly useful in helping make or rule out the diagnosis.[45]
Echocardiography is the main type of diagnostic imaging used to establish the diagnosis of infective endocarditis.[11] There are two main types of echocardiography used to assist with the diagnosis of IE: transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE).[11]
The transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probable' or 'almost certain' evidence of endocarditis.[46][47] However, in endocarditis involving a prosthetic valve, TTE has a sensitivity of approximately 50%, whereas TEE has a sensitivity exceeding 90%.[11] The TEE also has an important diagnostic role when the TTE does not reveal IE but diagnostic suspicion remains high, since TEE is more sensitive for infective endocarditis and is better able to characterize infection-related damage to the heart valves and surrounding tissues.[11]
Guidelines support the initial use of TTE over TEE in people with abnormal blood cultures, a new heart murmur, and suspected infective endocarditis.[11] TEE is the preferred initial form of imaging in people with suspected infective endocarditis who have a moderate to high pretest probability of infective endocarditis, including people with prosthetic heart valves, blood cultures growingStaphylococcus, or have an intracardiac device (such as apacemaker).[11]
Established in 1994 by the Duke Endocarditis Service and revised in 2000, the Duke criteria are a collection of major and minor criteria used to establish a diagnosis of infective endocarditis.[39][50] According to the Duke criteria, diagnosis of infective endocarditis can be definite, possible, or rejected.[38] A diagnosis of infective endocarditis is definite if either the following pathologicalor clinical criteria are met:
One of these pathological criteria:
One of these combinations of clinical criteria
Diagnosis of infective endocarditis is possible if one of the following combinations of clinical criteria is met:
Positive blood culture with typical IE microorganism, defined as one of the following:[38]
Evidence of endocardial involvement with a positive echocardiogram is defined as
Updated (2023) Modified Duke Criteria for Infective Endocarditis: Infective endocarditis (IE) is a life-threatening condition, and the Duke criteria (established in 1994 and revised in 2000) have been fundamental for the diagnosis of the disease. However, the landscape of microbiology, diagnostics, epidemiology, and treatment for IE has evolved significantly over the years. The 2023 modified Duke criteria address these changes:Updated (2023) Modified Duke Criteria for Infective Endocarditis
Among people who do notuse intravenous drugs and have a fever in theemergency department, there is a less than 5% chance of occult endocarditis. Mellors in 1987 found no cases of endocarditis nor of staphylococcal bacteremia among 135 febrile patientsin the emergency room.[44] The upperconfidence interval for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici found that among 113 non-selected adultsadmitted to the hospital because of fever, there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.[43]
Among people who do use intravenous drugs and have a fever in the emergency department, there is about a 10% to 15% prevalence of endocarditis. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever.[42] Weisse found that 13% of 121 patients had endocarditis.[40] Marantz also found a prevalence of endocarditis of 13% among such patients in the emergency department with fever.[42] Samet found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.[41] During theOpioid epidemic in the United States, hospitals observed an increase instroke associated with infective endocarditis.[51]
Among people with staphylococcal bacteremia (SAB), one study found a 29% prevalence of endocarditis in community-acquired SAB versus 5% in nosocomial SAB.[52] However, only 2% of strains were resistant to methicillin and so these numbers may be low in areas of higher resistance.[citation needed]
Not all people with heart disease require antibiotics to prevent infective endocarditis. Heart diseases have been classified into high, medium, and low risk of developing IE. Those falling into the high-risk category require IE prophylaxis before endoscopies and urinary tract procedures.Diseases listed under high risk include:[7]
The following are the antibiotic regimens recommended by the American Heart Association for antibiotic prophylaxis:[35]
In the UK, NICE clinical guidelines no longer advise prophylaxis because there is no clinical evidence that it reduces the incidence of IE, and there are negative effects (e.g., allergy and increased bacterial resistance) of taking antibiotics that may outweigh the benefits.[53]
Antibiotics were historically commonly recommended to prevent IE in those with heart problems undergoing dental procedures (known asdental antibiotic prophylaxis). There is, however, insufficient evidence to support whether antibiotics are effective or ineffective at preventing IE when given prior to a dental procedure in people at high risk.[54] They are less commonly recommended for this procedure.[55]
In some countries, e.g., the US, high-risk patients may be given prophylactic antibiotics such aspenicillin orclindamycin for penicillin-allergic people before dental procedures.[25] Prophylactics should bebactericidal rather thanbacteriostatic.[25] Such measures are not taken in certain countries e.g. Scotland due to the fear ofantibiotic resistance.[56] Because bacteria are the most common cause of infective endocarditis, antibiotics such aspenicillin[25] andamoxicillin (forbeta lactamase-producing bacteria) are used in prophylaxis.[citation needed]
High-doseantibiotics are the cornerstone of treatment for infective endocarditis. These antibiotics are administered by the intravenous (IV) route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adhering to them are supplied by blood vessels. Antibiotics are typically continued for two to six weeks, depending on the characteristics of the infection and the causativemicroorganisms. Antibiotic treatment lowers the risk of embolic complications in people with infective endocarditis.[11]
In acute endocarditis, due to the fulminant inflammation, empirical antibiotic therapy is started immediately after the blood has been drawn forculture to clarify the bacterial organisms responsible for the infection. This usually includesvancomycin andceftriaxone IV infusions until the infecting organism is identified and the susceptibility report with theminimum inhibitory concentration becomes available. Once this information is available, this allows the supervising healthcare professional to modify the antimicrobial therapy to target the specific infecting microorganism. The routine use of gentamicin to treat endocarditis has fallen out of favor due to the lack of evidence to support its use (except in infections caused byEnterococcus and nutritionally variantstreptococci) and the high rate of complications.[57] In cases of subacute endocarditis, where the person's hemodynamic status is usually stable, antibiotic treatment can be delayed until the causative microorganism can be identified.[citation needed]
Viridans groupstreptococci andStreptococcus bovis are usually highly susceptible to penicillin and can be treated with penicillin or ceftriaxone.[58] Relatively resistant strains ofviridans groupstreptococci andStreptococcus bovis are treated with penicillin or ceftriaxone along with a shorter two-week course of anaminoglycoside during the initial phase of treatment.[58] Highly penicillin-resistant strains of viridans groupstreptococci, nutritionally variantstreptococci likeGranulicatella sp.,Gemella sp.,Abiotrophia defectiva,[59] andEnterococci are usually treated with a combination therapy consisting of penicillin and an aminoglycoside for the entire duration of 4–6 weeks.[58]
Some people may be treated with a relatively shorter course of treatment[58] (two weeks) with benzyl penicillin IV if infection is caused by viridans groupstreptococci orStreptococcus bovis as long as the following conditions are met:
Additionally, oxacillin-susceptibleStaphylococcus aureus native valve endocarditis of the right side can also be treated with a short 2-week course of abeta-lactam antibiotic such asnafcillin with or without aminoglycosides.
The main indication for surgical treatment isregurgitation orstenosis. In active infective endocarditis, the surgery should remove enough leaflet tissue to ensure eradication of the infectious process.[60] Subsequent valve repair can be performed in limited disease.[60] Replacement of the valve with a mechanical or bioprostheticartificial heart valve is necessary in certain situations:[61]
The guidelines were recently updated by both theAmerican College of Cardiology and theEuropean Society of Cardiology. There was a recent meta-analysis published that showed surgical intervention at seven days or less is associated with lower mortality.[62]
Infective endocarditis is associated with 18% in-hospital mortality.[24] However, adult patients with congenital heart disease can have relatively lower mortality, down to 5% due to younger age, right-sided endocarditis, and management by multidisciplinary teams. As many as 50% of people with infective endocarditis may experience embolic complications.[11]
Indeveloped countries, the annualincidence of infective endocarditis is 3 to 9 cases per 100,000 persons.[38] Infective endocarditis occurs more often in men than in women.[11] There is an increased incidence of infective endocarditis in persons 65 years of age and older, which is probably because people in this age group have a larger number of risk factors for infective endocarditis. In recent years, over one-third of infective endocarditis cases in the United States washealthcare-associated.[38] Another trend observed in developed countries is that chronicrheumatic heart disease accounts for less than 10% of cases. Although a history of valve disease has a significant association with infective endocarditis, 50% of all cases develop in people with no known history of valvular disease.[citation needed]
Few diseases present greater difficulties in the way of diagnosis than malignant endocarditis, difficulties which in many cases are practically insurmountable. It is no disparagement to the many skilled physicians who have put their cases upon record to say that, in fully one-half, the diagnosis was made post mortem.
— William Osler, 1885
Lazare Riviére first described infective endocarditis affecting theaortic valve in 1616.[11] In 1806,Jean-Nicolas Corvisart coined the termvegetation to describe collections of debris found on a mitral valve affected by infective endocarditis.[11] The BritishphysicianJoseph Hodgson was the first to describe the embolic complications of infective endocarditis in 1815.[11] It was not until 1878 thatTheodor Klebs first suggested that infective endocarditis had a microbial infectious origin.[11] In 1909,William Osler noted that heart valves that experienced degeneration and were sclerotic or poorly functioning had a higher risk of being affected.[11] Later, in 1924,Emanuel Libman and Benjamin Sacks described cases ofvegetative endocarditis that lacked a clear microbial origin and were often associated with the autoimmune conditionsystemic lupus erythematosus.[11] In 1944, physicians reported on the first successful use ofpenicillin to treat a case of infective endocarditis.[11]
{{cite journal}}: CS1 maint: DOI inactive as of July 2025 (link)
