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|Classification and external resources|
A mitral valve vegetation caused by bacterial endocarditis.
|Classification and external resources|
A mitral valve vegetation caused by bacterial endocarditis.
Infective endocarditis is a form of endocarditis, or inflammation, of the inner tissue of the heart (such as its valves) caused by infectious agents. The agents are usually bacterial, but other organisms can also be responsible.
The valves of the heart do not receive any dedicated blood supply. As a result, defensive immune mechanisms (such as white blood cells) cannot directly reach the valves via the bloodstream. If an organism (such as bacteria) attaches to a valve surface and forms a vegetation, the host immune response is blunted. The lack of blood supply to the valves also has implications for treatment, since drugs also have difficulty reaching the infected valve.
Historically, infective endocarditis has been clinically divided into acute and subacute presentations (because untreated patients tended to live longer with the subacute as opposed to the acute form). This classifies both the rate of progression and severity of disease.
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 terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred.
Infective endocarditis may also be classified as culture-positive or culture-negative. By far the most common cause of a "culture-negative" endocarditis is prior administration of antibiotics.
Sometimes micro-organisms can take a longer period of time to grow in the culture media, such organisms are said to be fastidious because they have demanding growth requirements. Some examples include pathogens like Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria. Due to delay in growth and identification in these cases, patients may be erroneously classified as "culture-negative" endocarditis.
Endocarditis can also be classified by the side of the heart affected:
Another form of endocarditis is healthcare associated endocarditis when the infecting organism is believed to be transmitted in a health care setting like 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 stay in a hospital and it is usually secondary to presence of intravenous catheters, Total parenteral nutrition lines, pacemakers, etc.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic valve endocarditis can be early (< 60 days of valvular surgery), intermediate (60 days to 1 year) or late (> 1 year following valvular surgery).
A common mnemonic for the signs and symptoms of endocarditis is FROM JANE:
Many microorganisms can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is removed, and any growth is noted and identified. The term bacterial endocarditis (BE) commonly is used, reflecting the fact that most cases of IE are due to bacteria; however, Infective Endocarditis (IE) has become the preferred terms.
Staphylococcus aureus followed by Streptococci of the viridans group and Coagulase negative Staphylococci are the three most common organisms responsible for infective endocarditis. OtherStreptococci and Enterococci are also a frequent cause of infective endocarditis. HACEK group of micro-organisms and Fungi are seen less frequently.
Viridans Alpha-hemolytic streptococci, that are present in the mouth are the most frequently isolated micro-organisms when the infection is acquired in a community setting. In contrast, Staphylococcus blood stream infections are frequently acquired in a health care setting where they can enter the blood stream through procedures that cause break in the integrity of skin like surgery, catheterisation or during access of long term indwelling catheters or secondary to intravenous injection of recreational drugs.
Enterococcus can enter the bloodstream as a consequence of abnormalities in the gastrointestinal or genitourinary tracts.
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 in literature. Few examples include: Propionibacterium sp., which are normal skin flora, have been responsible for infective endocarditis sometimes leading to deaths due to the indolent course of this abscess producing infection.Tropheryma whipplei has caused endocarditis without gastrointestinal involvement. Citrobacter koseri was found in an immunocompetent adult. Neisseria bacilliformis was found in a patient with a bicuspid aortic valve.
Candida albicans, a yeast, is associated with endocarditis in IV drug users and immunocompromisedpatients. Other fungi demonstrated to cause endocarditis are Histoplasma capsulatum and Aspergillus. Endocarditis with Tricosporon asahii has also been reported in a case report.
In a healthy individual, a bacteremia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with a piece of blood clot, the valve provides a place for the bacteria to attach themselves and an infection can be established.
In the past, bacteremia caused by dental procedures (in most cases due to streptococci viridans, which reside in oral cavity), such as a cleaning or extraction of a tooth was thought to be more clinically significant than it actually was. However, it is important that a dentist or a dental hygienist be told of any heart problems before commencing treatment. Antibiotics are administered to patients with certain heart conditions as a precaution, although this practice has changed in the US, with new American Heart Association guidelines released in 2007, and in the UK as of March 2008 due to new NICE guidelines. Everyday tooth brushing and flossing will similarly cause bacteremia. Although there is little evidence to support antibiotic prophylaxis for dental treatment, the current American Heart Association guidelines are highly accepted by clinicians and patients.
Other conditions that result in high number of bacteria entering into the bloodstream include colorectal cancer (mostly Streptococcus bovis), serious urinary tract infections (mostly enterococci), and drug injection (Staphylococcus aureus). With a large number of bacteria, even a normal heart valve may become infected.
A more virulent organism (such as Staphylococcus aureus) can cause infective endocarditis by infecting even a normal heart valve.
Intravenous drug users tend to get their right-sided heart valves infected because the veins that are injected drain into the right side of the heart. In rheumatic heart disease, infection occurs on the aortic and the mitral valves on the left side of the heart.
As previously mentioned, altered blood flow around the valves contributes to development of endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve leads to formation of a local blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE). Altered blood flow, and thus infective endocarditis, are more likely in high pressure areas. Consequently, ventricular septal defects create more susceptibility than atrial septal defects. Damaged vascular endothelium will also promote platelet and fibrin deposition, upon which bacteria can take hold. Valvular lesions are a major cause of such damage, as are jet lesions resulting from ventricular septal defects or patent ductus arteriosus.
In general, the Duke criteria should be fulfilled in order to establish the diagnosis of endocarditis. The blood tests C reactive protein (CRP) and procalcitonin have not been found to be particularly useful in helping make or rule out the diagnosis.
As the Duke criteria rely heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among patients with intravenous drug abuse and among non drug-abusing patients. Unfortunately, this research is over 20 years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococci make the following estimates incorrect.
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.
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 endocarditis. A definite diagnosis of infective endocarditis can be established if the following conditions are fulfilled: two major criteria, one major and three minor criteria, or five minor criteria. Diagnosis of infective endocarditis can only be said to be "possible" if only 1 major and 1 minor criteria are fulfilled or if only 3 minor criteria are fulfilled.
Major criteria include:
Minor criteria include:
Among people who do not use intravenous drugs and have a fever in the emergency room, 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 patients in the emergency room. The upper confidence 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 adults admitted to the hospital because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.
Among people who do use intravenous drugs and have a fever in the emergency room, 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. Weisse found that 13% of 121 patients had endocarditis. Marantz also found a prevalence of endocarditis of 13% among such patients in the emergency room with fever. 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.
Among people with staphylococcal bacteremia (SAB), one study found a 29% prevalence of endocarditis in community-acquired SAB versus 5% in nosocomial SAB. However, only 2% of strains were resistant to methicillin and so these numbers may be low in areas of higher resistance.
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 high risk category require IE prophylaxis before endoscopies and urinary tract procedures. Diseases listed under high risk include
Following are the antibiotic regimens recommended by the American Heart Association for antibiotic prophylaxis:
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.
Antibiotics were historically commonly recommended to prevent IE in those with heart problems undergoing dental procedures (known as dental antibiotic prophylaxis). They are less commonly recommended for this procedure.
High dose antibiotics are administered by the intravenous 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 adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks depending on the characteristics of the infection and the causative micro-organisms.
In acute endocarditis, due to the fulminant inflammation empirical antibiotic therapy is started immediately after the blood has been drawn for culture. This usually includes vancomycin and ceftriaxone IV infusions until the microbial identification and susceptibility report with the minimum inhibitory concentration becomes available allowing for modification of the antimicrobial therapy to target the specific microorganism. It should be noted that 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 by Enterococcus and nutritionally variant streptococci) and the high rate of complications.
The most common organism responsible for infective endocarditis is Staphylococcus aureus, which is resistant to penicillin in most cases. High rates of resistant to oxacillin are also seen, in which cases treatment with vancomycin is required.
Relatively resistant strains of viridans group streptococci and Streptococcus bovis are treated with penicillin or ceftriaxone along with a shorter 2 week course of an aminoglycoside during the initial phase of treatment.
Highly penicillin resistant strains of viridans group streptococci, nutritionally variant streptococci like Granulicatella sp., Gemella sp. and Abiotrophia defectiva, and Enterococci are usually treated with a combination therapy consisting of penicillin and an aminoglycoside for the entire duration of 4–6 weeks.
Selected patients may be treated with a relatively shorter course of treatment (2 weeks) with benzyl penicillin IV if infection is caused by viridans group streptococci or Streptococcus bovis as long as the following conditions are met:
Additionally oxacillin susceptible Staphylococcus aureus native valve endocarditis of the right side can also be treated with a short 2 week course of beta lactam antibiotic like nafcillin with or without aminoglycosides
‣ Patients with significant valve stenosis or regurgitation causing heart failure ‣ Evidence of hemodynamic compromise in the form of elevated end diastolic left ventricular or left atrial pressure or moderate to severe pulmonary hypertension ‣ Presence of intracardiac complications like paravalvular abscess, conduction defects or destructive penetrating lesions ‣ Recurrent septic emboli despite appropriate antibiotic treatment ‣ Large vegetations (> 10 mm) ‣ Persistent positive blood cultures despite appropriate antibiotic treatment ‣ Prosthetic valve dehiscence ‣ Relapsing infection in the presence of a prosthetic valve ‣ Abscess formation ‣ Early closure of mitral valve ‣ Infection caused by Fungi or resistant Gram negative bacteria
Infective endocarditis is associated with 18% in-hospital mortality.