Infective endocarditis

Last updated: April 29, 2022

Summarytoggle arrow icon

Infective endocarditis (IE) is an infection of the endocardium that typically affects one or more heart valves. The condition is usually a result of bacteremia, which is most commonly caused by dental procedures, surgery, distant primary infections, and nonsterile injections. IE may be acute (developing over hours or days) or subacute (progressive over weeks to months). Acute bacterial endocarditis is usually caused by Staphylococcus aureus and leads to rapid destruction of endocardial tissue, while subacute bacterial endocarditis is most commonly caused by viridans streptococci and generally affects individuals with preexisting damage to the heart valves, structural heart defects, or prosthetic valves. Clinical features include constitutional symptoms (fatigue, fever/chills, malaise), signs of pathological cardiac changes (e.g., new or changed heart murmur, heart failure signs), and, in some cases, manifestations of subsequent damage to other organs (e.g., glomerulonephritis, septic embolic stroke). Management is complex and infectious disease specialists should be involved early. Diagnosis is made based on the Duke criteria, the main features of which are positive blood cultures and evidence of endocardial involvement on echocardiography. Initial treatment of IE consists of empiric IV antibiotics, which are then adapted according to blood culture results and continued for several weeks. Categorization into native valve endocarditis or prosthetic valve endocarditis helps to further tailor regimens. Surgery may be necessary in complex cases (e.g., valve perforation). IE prophylaxis is administered in specific circumstances, e.g., in patients with congenital heart disease having certain dental procedures. IE is typically fatal if left untreated.

Pathogens

Pathogens causing infective endocarditis (IE)
Main pathogens Characteristics

Staphylococcus aureus

  • Approximately 35–40% of native valve IE cases [1]
  • Most common cause of acute IE, including persons who inject drugs and patients with prosthetic valves or pacemakers/ICDs [2][3]
  • Typically affects healthy valves.
  • Usually fatal within 6 weeks if left untreated

Viridans streptococci

Staphylococcus epidermidis

Enterococci (especially Enterococcus faecalis)

  • Approximately 10% of native valve IE cases [1]
  • Multiple drug resistance
  • Common cause of IE following nosocomial UTIs
  • Causes native and prosthetic valve IE
  • Following gastrointestinal or genitourinary procedures

Streptococcus gallolyticus subsp. gallolyticus (Sgg) [5]

Gram-negative HACEK group

  • Less than 5% of native valve IE cases [1][6]
  • Physiological oral pharyngeal flora
  • In patients with poor dental hygiene and/or periodontal infection

Fungal endocarditis (Candida, Aspergillus fumigatus) [7][8]

  • Less than 5% of native valve IE cases [1]
  • At risk groups

Coxiella burnetii

Bartonella species

  • Less than 5% of native valve IE cases [1]
  • Gram-negative pathogens responsible for culture-negative endocarditis

Risk factors for infective endocarditis [1][4][10]

“Don't tri drugs for the sake of your tricuspid valves.”

Constitutional symptoms [1][12]

Patients with subacute IE often present with nonspecific flu-like symptoms, while patients with acute IE often present with signs of acute sepsis.

A high index of suspicion is required in patients with risk factors for IE, as classic extracardiac manifestations (e.g., splinter hemorrhages, Janeway lesions) are absent in the majority of patients. [6][13]

Cardiac manifestations [1][12]

Extracardiac manifestations of IE [1][12]

Extracardiac manifestations are typically caused by septic microemboli and/or immune complex precipitation and are more commonly seen in left-sided IE, with the exception of pulmonary embolic manifestations, which are more common in right-sided IE. [1][15]

Up to one-third of patients with left-sided IE present with symptoms of stroke. [18]

IE should always be considered as a cause of fever of unknown origin (FUO), especially in the presence of a new heart murmur.

FROM JANE:” Features of IE include Fever, Roth spots, Osler nodes, Murmur, Janeway lesions, Anemia, Nail bed hemorrhage, and Emboli.

  • IE can be classified by:
    • Type of affected valve (native vs. prosthetic)
    • Acuity of the infection
    • Location of the infection (left- vs. right-sided).
  • Although this is not a definitive classification system, it can help in the approach to management and selection of empiric antibiotic regimens.

Classification by valve type and duration of infection

Classified by type of valve involved and clinical course [15]
Native valve endocarditis Prosthetic valve endocarditis
Acute bacterial endocarditis Subacute bacterial endocarditis
Clinical features
  • Early-onset: ≤ 1 year after surgery
  • Late-onset: > 1 year after surgery
Main pathogens
  • Most common: S. aureus (associated with large vegetations that can destroy the valves)
  • Others: group A hemolytic streptococci, S.pneumoniae, N.gonorrhoeae
Affected valves
  • Healthy native valves
  • Native valves with prior injury or congenital defects

Classification by location

Classified by location of valves involved
Right-sided endocarditis [20] Left-sided endocarditis [15]
Distinguishing clinical features
Main pathogens
Affected valves
  • Tricuspid
  • Pulmonic
  • Mitral
  • Aortic

Approach [15][21]

  • Suspect IE based on clinical findings (e.g., fever without focus combined with a new murmur) and predisposing conditions.
  • The modified Duke criteria help categorize the diagnostic likelihood of IE: definite vs. possible vs. rejected. [6]
    • Used as a diagnostic guide; not a substitute for clinical judgment
    • Incorporate clinical, microbiological, pathological, and imaging criteria.
  • All patients should receive multiple blood cultures and echocardiography.
  • Obtain ECG and additional imaging to investigate any complications or new focal symptoms or signs of metastatic infection.
  • Consider serology to evaluate blood culture-negative endocarditis.
  • Consult infectious disease (ID) if the diagnosis is uncertain.

Draw three sets of blood cultures, each from a different venipuncture site, as soon as IE is suspected, preferably before antibiotic treatment is initiated.

Modified Duke criteria [6][15][22]
Criteria Findings
Major
Minor
  • Predisposing condition (e.g., underlying heart abnormality, IV drug use) [23]
  • Fever > 38°C (100.4°F)
  • Vascular abnormalities
  • Immunologic phenomena
  • Microbiology: positive blood cultures not fulfilling major criteria or serological evidence of infection with common organisms
Pathological
  • Microorganisms demonstrated by tissue culture or histology
  • Characteristic histologic features of active endocarditis

Diagnostic category
Definite IE
if any of the following are present:
≥ 2 major criteria
≥ 1 major criterion PLUS ≥ 3 minor criteria
≥ 5 minor criteria

≥ 1 pathological criterion
Possible IE if any of the following are present:
≥ 1 major criterion PLUS ≥ 1 minor criterion
≥ 3 minor criteria
Rejected diagnosis if:
Criteria for definite or possible IE not fulfilled
Firm alternative diagnosis present
Resolution of clinical characteristics in ≤ 4 days of antimicrobial therapy
Absence of surgical or autopsy evidence of IE

Laboratory studies [15]

Routine studies

Blood cultures [25]

See also “Intravascular catheter-related bloodstream infections” and “Bacteremia.”

Negative blood cultures do not rule out IE. A significant proportion of patients with IE have sterile cultures.

Echocardiography [15]

Transthoracic echocardiography (TTE) is the initial test of choice for all patients with suspected IE. It should ideally be performed within 12 hours of presentation and repeated after completing treatment. Transesophageal echocardiography (TEE) is more invasive and is added in select cases. [15]

  • Indications for TEE include:
    • Presence of high-risk features
    • TTE findings inconclusive or suggestive of IE
    • Preoperative planning
    • Concern for intracardiac complications (e.g., abscess)
  • Echocardiographic findings fulfilling Duke criteria for IE: similar in TTE and TEE [6][27][28]
  • Other high-risk findings include:

TEE is more sensitive (∼ 90%) than TTE (∼ 75%) and is more reliable in ruling out IE in patients with moderate-to-high pretest probability.

Additional investigations [15][25]

Obtain an ECG in all patients with suspected IE to assess for new conduction abnormalities (e.g., AV block, bundle branch block) that suggest the development of a perivalvular or myocardial abscess. Consider urgent cardiac imaging (e.g., TEE, cardiac MRI) if these abnormalities are present. [6][21]

  • Acute disease (leading to valve insufficiency, septic embolic infarcts, tendinous cord rupture) [31]
  • Chronic disease (leading to valve insufficiency and valve stenosis) [31]

Noninfective endocarditis (nonbacterial thrombotic endocarditis) [32][33]

Prosthetic valve thrombosis [35]

The differential diagnoses listed here are not exhaustive.

Initial management [6][15][36][37]

If IE is suspected, first obtain blood cultures, then consult infectious disease to plan empiric antibiotic therapy. When culture results are available, adapt the therapy accordingly.

Supportive care

Antibiotics

Empiric antibiotic therapy [15]

The goal is to provide broad-spectrum coverage for potential bacterial causes of IE (including multidrug-resistant organisms) until blood culture results are available.

Empiric antibiotic therapy for infective endocarditis [15]
Valve type Clinical presentation Common regimen
Native valve endocarditis Acute bacterial endocarditis (days)
Subacute bacterial endocarditis (weeks)
Prosthetic valve endocarditis ≤ 1 year after valve placement
> 1 year after valve placement

Targeted antibiotic therapy [15]

Targeted antibiotic therapy based on culture and sensitivity results is recommended for all patients with IE.

Targeted antimicrobial therapy for infective endocarditis [15]
Organism Native valve endocarditis (common regimens) Prosthetic valve endocarditis (common regimens)
Methicillin-susceptible staphylococci (e.g., MSSA)
Methicillin-resistant staphylococci (e.g., MRSA)
Viridans group streptococci, S. gallolyticus
Enterococcus spp. (penicillin-sensitive)
Enterococcus spp. (penicillin-resistant)
HACEK

Surgery [15][36][38]

These procedures typically follow a multidisciplinary decision made by cardiology, cardiothoracic surgery, and infectious disease services.

Surgical intervention is required in 50–60% of patients with IE. [38]

Unstable patients

All patients

We list the most important complications. The selection is not exhaustive.

Endocarditis prophylaxis [36][44][45][46]

Prophylaxis is indicated prior to certain procedures with a high risk of bacteremia in patients with high-risk cardiac features. [44]

IE prophylaxis is not routinely recommended prior to nondental procedures (including respiratory, skin, musculoskeletal, gastrointestinal, and genitourinary procedures) unless infected tissue is present. [36]

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