B.30 Infective Endocarditis Flashcards
B.30 Infective Endocarditis
definiton
Infective endocarditis (IE) is infection of the endocardial surface of the heart, typically involving heart valves, caused by bacteria or fungi.
Infective endocarditis (IE) is an infection of the endocardium that typically affects one or more heart valves. The condition is usually due to bacteremia, which is most commonly caused by dental procedures, surgery, distant primary infections, and nonsterile injections.
B.30 Infective Endocarditis
what are the main pathogens
Staphylococcus aureus (45-65%)
Viridans Streptococcus (30%): includes S. sanguinis, S. mutans, S. milleri
Staphylococcus epidermidis
Enterococci, particularly Enterococcus faecalis (≈ 10%)
Streptococcus gallolyticus (S. bovis)
Gram-negative HACEK group: Aggregatibacter aphrophilus, Cardiobacterium hominis, Eikenella corrodens, Kingella species,
Candida species: Aspergillus fungus
Bartonella species, Coxiella burnetii
B.30 Infective Endocarditis
Staphylococcus aureus
The primary cause of acute infective endocarditis (IE) across all demographics, including intravenous drug users and individuals with prosthetic valves or implantable cardioverter-defibrillators (ICDs).
Affects valves that were previously healthy.
Typically results in a fatal outcome within 6 weeks if not treated.
B.30 Infective Endocarditis
Viridans streptococci (30%): Includes S. sanguinis, S. mutans, and S. mitis.
The leading cause of subacute infective endocarditis (IE), particularly in pre-existing damaged native valves (primarily the mitral valve).
A frequent cause of IE after dental procedures.
Produces dextrans that help bind fibrin-platelet aggregates to damaged heart valves.
B.30 Infective Endocarditis
Staphylococcus epidermidis
Infective endocarditis (IE) can be transmitted through infected peripheral venous catheters.
A common cause of subacute IE in patients with prosthetic heart valves or pacemakers/ICDs.
B.30 Infective Endocarditis
Enterococci, particularly Enterococcus faecalis (≈ 10%)
Presence of multiple drug resistance.
A frequent cause of infective endocarditis (IE) after nosocomial urinary tract infections (UTIs).
Occurs after gastrointestinal (GI) or genitourinary (GU) procedures.
B.30 Infective Endocarditis
Streptococcus gallolyticus (S. bovis)
S. gallolyticus is linked to colorectal cancer.
If S. gallolyticus is identified, a colonoscopy is recommended.
B.30 Infective Endocarditis
Gram-negative HACEK group: Aggregatibacter aphrophilus, Cardiobacterium hominis, Eikenella corrodens, Kingella species
Physiological oropharyngeal flora accounts for approximately 3% of infective endocarditis (IE) cases.
This is seen in individuals with inadequate dental hygiene and/or periodontal infections.
B.30 Infective Endocarditis
Candida species: Aspergillus fungus
Infective endocarditis (IE) can occur in immunosuppressed individuals.
IE is also seen in intravenous drug users.
Additionally, it can develop following cardiac surgical procedures.
B.30 Infective Endocarditis
Bartonella species, Coxiella burnetii
Gram-negative bacteria associated with culture-negative endocarditis.
B.30 Infective Endocarditis
Risk Factors
Demographics
Male sex
Age > 60 years
Cardiac conditions
Acquired valvular disease (e.g., rheumatic heart disease, aortic stenosis, degenerative valvular disease)
Prosthetic heart valves
Congenital heart defects (e.g., VSD, bicuspid aortic valve)
Previous IE
Cardiac implantable electronic device (CIED)
Noncardiac risk factors
Poor dental status
Dental procedures
Nonsterile venous injections (e.g., in IV drug use)
Intravascular devices
Surgery
Chronic hemodialysis
Immunocompromise (e.g., HIV infection, diabetes)
Other bacterial infections (e.g., UTIs, spondylodiscitis, periodontal infection)
B.30 Infective Endocarditis
Pathophys
Pathogenesis
Damaged valvular endothelium → exposure of the subendothelial layer → adherence of platelets and fibrin → sterile vegetation (microthrombus)
Undamaged native valves are usually not susceptible to either thrombus formation or colonization by most types of bacteria (except for S. aureus).
Localized infection or contamination → bacteremia → bacterial colonization of vegetation → formation of fibrin clots encasing the vegetation → valve destruction with loss of function (valve regurgitation)
Valve involvement
Frequency of valve involvement: mitral valve > aortic valve > tricuspid valve > pulmonary valve
The tricuspid valve is the most commonly affected valve in individuals who inject drugs (associated with Pseudomonas, S. aureus, and Candida).
Clinical consequences
Bacterial vegetation → bacterial thromboemboli → vessel occlusion → infarctions
Emboli can lead to metastatic infections of other organs.
Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes
B.30 Infective Endocarditis
Clinical Features
Fever and chills (seen in ∼ 90% of patients)
Tachycardia
General malaise, weakness, weight loss, night sweats
Dyspnea, cough, pleuritic chest pain
Arthralgias, myalgias
Patients with subacute IE often present with nonspecific flu-like symptoms, while patients with acute IE often present with signs of acute sepsis.
B.30 Infective Endocarditis
Cardiac Manifestations
New Heart Murmur: Development or alteration of an existing murmur.
Mitral Valve Regurgitation
Tricuspid Valve Regurgitation: Commonly observed in IV drug users and individuals with concurrent HIV infection, immunosuppressed patients, and those with central venous catheters.
Aortic Valve Regurgitation
Signs of Progressive Heart Failure: Symptoms may include dyspnea and edema.
Signs of Acute Cardiac Decompensation: Such as pulmonary edema.
Arrhythmias: Consider the possibility of perivalvular abscess in patients with infective endocarditis who experience new conduction abnormalities (e.g., third-degree atrioventricular block).
B.30 Infective Endocarditis
Course of the Disease
Acute Bacterial Endocarditis: Rapid onset and severe progression within days to weeks, often accompanied by significant constitutional symptoms such as high fever.
Subacute Bacterial Endocarditis: Characterized by a gradual onset and slower progression over weeks to months, typically exhibiting milder constitutional symptoms, including the possibility of low-grade fever or no fever at all.
Prosthetic Valve Endocarditis:
Early Onset: Occurs within 60 days post-surgery.
Late Onset: Develops more than 60 days after surgery.
B.30 Infective Endocarditis
Extracaardiac Manifestations
These manifestations are primarily due to bacterial microemboli and/or the formation of immune complexes.
Janeway Lesions:
- Small, non-tender, erythematous macules on the palms and soles.
- Associated with microabscesses and capillary infiltration, resulting in hemorrhage from targeted microorganisms at valve locations.
Osler Nodes:
- Painful nodules located on the pads of the fingers and toes.
- Caused by immune complex deposition.
Roth Spots:
- Retinal hemorrhages with pale centers, indicating underlying vascular issues.
Signs of Acute Renal Injury:
- May include hematuria and anuria due to renal artery obstruction or glomerulonephritis.
Splenomegaly and possible left upper quadrant (LUQ) pain.
Neurological Manifestations:
Such as seizures and paresis, resulting from septic embolic stroke, hemorrhages, meningitis, encephalitis, or abscess.
Signs of Pulmonary Embolism:
Symptoms like dyspnea, typically arising from septic emboli associated with tricuspid valve involvement.
B.30 Infective Endocarditis
Lab DX
Best Initial Test:
Multiple blood cultures.
Note: Coxiella burnetti and Bartonella spp. often yield negative cultures.
Leukocytosis:
Often present (with a left shift), along with elevated ESR and CRP.
B.30 Infective Endocarditis
Echocardiography DX
Detects:
Valve vegetations, new valvular regurgitation, abscesses, and dehiscence of prosthetic valves.
Transthoracic Echocardiography (TTE):
Typically performed first; sensitivity is about 75%.
Transesophageal Echocardiography (TEE):
Used for confirmation; has a higher sensitivity (> 90%) compared to TTE.
B.30 Infective Endocarditis
Modify Duke’s Criteria
To confirm the diagnosis, one of the following must be met:
Two Major Criteria
One Major and Three Minor Criteria
Five Minor Criteria
Major Diagnostic Criteria:
1. Two separate blood cultures positive for typical pathogens
2. Evidence of endocardial involvement in echocardiography:
- Valve vegetation or abscess, or new dehiscence of artificial valves.
- New valvular regurgitation (worsening of a pre-existing murmur is not sufficient).
Minor Diagnostic Criteria:
1. Predisposition: Underlying heart disease or IV drug use
2. Fever: Temperature ≥ 38°C
3. Vascular Abnormalities:
- Arterial emboli, septic infarcts, and intracranial hemorrhages
4. Immunologic Disorders:
- Glomerulonephritis, Osler’s nodes, Roth spots, and positive rheumatoid factor
5. Microbiology: Positive blood cultures for atypical pathogens other than the ones typically identified.
B.30 Infective Endocarditis
Preventative TX
Indications: Recommended for high-risk patients undergoing procedures that may lead to bacteremia.
Regimens:
Usually Oral Amoxicillin (administer 1 hour prior to the procedure)
For patients unable to take oral medication: IV Ampicillin
For patients with a penicillin allergy: Oral Clarithromycin or Azithromycin
B.30 Infective Endocarditis
AB TX for Native Valves:
Empiric Therapy: Start with intravenous vancomycin and adjust antibiotic therapy based on blood culture results.
Duration: Treatment length varies based on the patient’s profile, pathogen resistance, and other factors.
4-Week Treatment:
Drug of Choice: Penicillin G
Alternatives: Ampicillin, IV Ceftriaxone, or IV Vancomycin
Treatment Regimens:
Preferred: Gentamicin + Penicillin G
Alternative: Gentamicin + Ceftriaxone
B.30 Infective Endocarditis
AB TX for Prosthetic Valves:
General Approach: Similar antibiotic regimen as for native valves, but with an extended duration of at least 6 weeks.
Exceptions for Staphylococci:
Methicillin-Susceptible:
Use Nafcillin (or Oxacillin, Cefazolin) + Rifampin + Gentamicin
Methicillin-Resistant:
Use Vancomycin + Rifampin + Gentamicin
B.30 Infective Endocarditis
AB TX for HACEK
Drug of Choice:
First-Line: 3rd or 4th generation IV cephalosporin (e.g., Ceftriaxone, Cefotaxime)
Second-Line: Ampicillin-sulbactam, IV Fluoroquinolone
Duration of Therapy:
Native Valve Infective Endocarditis: 4 weeks
Prosthetic Valve Infective Endocarditis: 6 weeks
B.30 Infective Endocarditis
Patient with fever and murmur has normal TTE. Can you rule out endocarditis?
→ ❌ No. TEE is required for better sensitivity, especially in prosthetic valves or high-risk patients.
B.30 Infective Endocarditis
aneway lesions are painful – true or false?
→ ❌ False. Janeway = painless, Osler = painful.
B.30 Infective Endocarditis
Does a single positive blood culture with Staph aureus always need full treatment for IE?
→ ✅ Yes. Staph aureus always means serious infection, even if only one bottle grows it.
B.30 Infective Endocarditis
Can right-sided endocarditis cause a stroke?
→ ❌ No – emboli go to lungs. Stroke = left-sided IE.
B.30 Infective Endocarditis
In a patient with a prosthetic valve and fever, can IE be diagnosed without a murmur?
→ ✅ Yes. Murmur may be absent or subtle. High suspicion → TEE and cultures are essential.
B.30 Infective Endocarditis
Why might creatinine rise in infective endocarditis?
→ Could be due to glomerulonephritis, drug toxicity (gentamicin), or embolic infarcts.
