Infective Endocarditis

Infective endocarditis is an infection of the endocardial surface of the heart, most often affecting the heart valves.

It typically arises when bacteria in the bloodstream adhere to an area of previously damaged or abnormal endothelium, then proliferate within a protective fibrin and platelet matrix known as a vegetation.

Risk factors include pre-existing valvular disease (native valve endocarditis), prosthetic heart valves (a particularly high risk group, further divided into early, within one year of surgery, and late presentations, since the causative organisms and management differ), intravenous drug use (classically causing right sided, tricuspid valve endocarditis), and intracardiac devices such as pacemakers.

• Staphylococcus aureus is now the leading overall cause in most series, and tends to cause a more acute, aggressive presentation.

• Viridans group streptococci, historically the dominant cause associated with dental procedures and pre-existing valve disease, tend to cause a more indolent, subacute course.

• Enterococci, particularly Enterococcus faecalis, are increasingly recognized, often following genitourinary or gastrointestinal procedures.

• The HACEK group of fastidious gram negative organisms and Coxiella burnetii (culture negative endocarditis) are less common but important considerations when standard blood cultures are repeatedly negative.

Presentation ranges from an indolent, subacute illness with low grade fever, malaise, weight loss, and night sweats over weeks, through to an acute, fulminant illness with high fever and rapid hemodynamic compromise, depending largely on the causative organism and any underlying valve abnormality.

A new or changing cardiac murmur is a key finding, though it may be absent early in the disease course.

Peripheral stigmata, while classic, are seen less frequently than in older teaching and reflect immune complex deposition and embolic phenomena: Janeway lesions (painless, erythematous macules on the palms and soles), Osler's nodes (painful, tender nodules on the finger and toe pads), splinter hemorrhages (linear hemorrhages under the nail bed), Roth spots (retinal hemorrhages with pale centers, seen on fundoscopy), and petechiae.

Embolic complications can affect virtually any organ and often dominate the clinical picture: stroke (from left sided vegetations), splenic infarction, renal infarction, and, in right sided endocarditis from intravenous drug use, septic pulmonary emboli causing cough, pleuritic pain, and multiple cavitating lesions on chest imaging. Glomerulonephritis from immune complex deposition can cause hematuria and renal impairment.

Diagnosis relies on the modified Duke criteria, which combine major and minor criteria.

• The major criteria are persistently positive blood cultures with a typical endocarditis organism, and evidence of endocardial involvement on echocardiography (a vegetation, abscess, new valvular regurgitation, or new dehiscence of a prosthetic valve).

• Minor criteria include predisposing heart condition or intravenous drug use, fever above 38 degrees Celsius, vascular phenomena (emboli, Janeway lesions, septic pulmonary infarcts), immunologic phenomena (Osler's nodes, Roth spots, glomerulonephritis, positive rheumatoid factor), and microbiological evidence not meeting the major criterion threshold.

Blood cultures are essential and should be taken as three separate sets from different venepuncture sites before starting antibiotics, since this single step most strongly determines whether a causative organism, and therefore targeted therapy, can be identified.

Transthoracic echocardiography is the first-line imaging study; transesophageal echocardiography has substantially higher sensitivity, particularly for prosthetic valves, smaller vegetations, and posterior structures, and should be performed if transthoracic imaging is negative or equivocal but clinical suspicion remains high.

Additional bloods include FBC (normocytic anemia, leukocytosis), inflammatory markers, and renal function (both as a baseline and to detect embolic or immune complex related renal injury).

Urinalysis assesses for hematuria from glomerulonephritis.

Differentials include other causes of fever with a heart murmur (rheumatic fever, atrial myxoma with embolic phenomena), other causes of culture negative fever, and other sources of bacteremia with an incidental pre-existing murmur.

Prolonged intravenous antibiotic therapy is the cornerstone of treatment, typically for four to six weeks, with the specific regimen guided by the causative organism and its susceptibility once identified.

Empirical therapy before cultures return, or in culture negative cases, is guided by whether the valve is native or prosthetic and the acuity of presentation, generally combining broad gram positive cover (such as vancomycin) with additional cover for gram negative and HACEK organisms as needed, per local protocol.

Surgery is indicated in a substantial proportion of cases and should not be delayed once a clear indication is present.

• Key indications include heart failure from severe valvular dysfunction, uncontrolled infection (perivalvular abscess, persistent bacteremia or fever despite appropriate antibiotics, fungal endocarditis), and prevention of embolism (large mobile vegetations, particularly with a prior embolic event).

• Timing of surgery relative to antibiotic course is individualized by a cardiology and cardiothoracic surgery team, balancing infection control against the risk of further embolic events if surgery is delayed.

Anticoagulation in a patient with a mechanical valve and endocarditis requires careful specialist input, balancing the competing risks of valve thrombosis against hemorrhagic transformation of an embolic stroke.

Prophylaxis with antibiotics before dental or other procedures is now reserved for a much narrower group than previously recommended, limited to those at highest risk of a poor outcome from endocarditis: patients with a prosthetic valve or prosthetic material used in valve repair, a prior episode of infective endocarditis, and certain forms of congenital heart disease. It is no longer recommended for the wider population of patients with native valve disease alone.

Referral: cardiology and cardiothoracic surgery for all confirmed or strongly suspected cases; infectious disease input is valuable for antibiotic selection and duration, particularly in culture negative or unusual organism cases.