Infective endocarditis (IE) is one of those Step topics that feels like “too many lists”… until you realize it’s really one story: endothelial damage → platelet-fibrin thrombus → bacteremia seeds it → vegetations → emboli + immune phenomena + valve destruction. If you can run that movie in your head, the murmurs, blood cultures, Duke criteria, and bug/drug pairings start to click fast.
Big-Picture Definition (What IE is)
Infective endocarditis = microbial infection of the endocardial surface, usually heart valves, leading to friable vegetations composed of:
- Fibrin + platelets
- Microorganisms
- Inflammatory cells (variable)
Key Step framing: IE is a valvular infection that causes:
- Regurgitant murmurs (valve destruction)
- Septic emboli (vegetations break off)
- Immune complex disease (glomerulonephritis, Osler nodes)
- Persistent bacteremia (positive blood cultures)
First Aid cross-reference: Cardiovascular → Endocarditis (classically near murmurs + embolic/immune findings + blood cultures + Duke).
Pathophysiology: The “2-Hit” Model You Should Memorize
Hit #1: Endothelial injury → “sterile” thrombus
Abnormal flow or trauma exposes subendothelial matrix → platelet + fibrin deposition → nonbacterial thrombotic endocarditis (NBTE) scaffold.
Common settings:
- Damaged valves (rheumatic disease, bicuspid aortic valve, degenerative calcific disease)
- Prosthetic valves
- Congenital heart disease
- IV drug use (particulate damage, frequent bacteremia)
Hit #2: Bacteremia → seeding → vegetations
Transient bacteremia (dental work, skin infection, IVDU, GU/GI procedures) allows organisms to adhere to fibrin/platelet nidus (think: adhesins).
High-yield mechanisms:
- Staph aureus can infect normal valves (very important)
- Viridans strep uses dextrans to stick to platelet-fibrin aggregates (classic board fact)
Classification: Acute vs Subacute (Step-Style)
| Feature | Acute IE | Subacute IE |
|---|---|---|
| Typical organisms | Staph aureus | Viridans strep, Enterococcus, HACEK |
| Valve status | Can involve normal valves | Usually abnormal valves |
| Clinical course | Rapid, toxic, destructive | Indolent, weeks–months |
| Complications | Abscesses, severe regurg, septic shock | Immune phenomena more noticeable |
Causative Organisms & Classic Associations (Extremely Testable)
Staph aureus
- IV drug users (classically tricuspid valve → septic pulmonary emboli)
- Acute IE, can infect normal valves
- Often large, destructive vegetations
Viridans streptococci
- Dental caries/procedures
- Subacute IE on damaged valves
- Dextran-mediated adherence (buzzword)
Staph epidermidis
- Prosthetic valve endocarditis
- Forms biofilms
- Early prosthetic infections (weeks–months) are commonly staph species
Enterococcus (E. faecalis, E. faecium)
- GU manipulation, elderly, urinary tract source
- Often requires synergistic therapy (classically a cell wall agent + aminoglycoside; resistance patterns matter clinically)
HACEK organisms
Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella
- Oropharyngeal flora
- Culture-negative or slow-growing endocarditis
- Classic treatment association: ceftriaxone
Culture-negative IE
Think:
- Prior antibiotics
- Fastidious organisms: Coxiella burnetii (Q fever; exposure to animals), Bartonella (homeless, lice; or cat exposure), HACEK
First Aid cross-reference: Microbiology → organism associations (viridans/dental, S. epidermidis/prosthetic, S. aureus/IVDU, enterococci/GU).
Clinical Presentation: What You Actually See
Core triad (board-style)
- Fever
- New or changing murmur (often regurgitant)
- Positive blood cultures (persistent bacteremia)
Vascular phenomena (embolic/septic)
- Janeway lesions: painless macules on palms/soles (septic microemboli)
- Splinter hemorrhages
- Septic emboli
- Left-sided IE → brain, kidney, spleen infarcts/abscesses
- Right-sided (tricuspid) → septic pulmonary emboli → pleuritic pain, hemoptysis, cavitary lesions
Immunologic phenomena
- Osler nodes: painful, tender nodules on fingers/toes (immune complex deposition)
- Roth spots: retinal hemorrhages with pale center
- Glomerulonephritis: hematuria, RBC casts, low complement (immune complex)
High-yield murmur patterns
- Mitral regurg: holosystolic murmur at apex radiating to axilla
- Aortic regurg: early diastolic decrescendo murmur along left sternal border
- IE can also cause valvular perforation, chordae rupture, and paravalvular abscess (especially aortic valve)
Diagnosis: Duke Criteria (Know the Logic, Not Just the List)
Initial tests you should think of immediately
- Blood cultures ×3 from different sites before antibiotics (if stable)
- Echocardiography
- Start with TTE
- Use TEE if prosthetic valve, high suspicion, poor TTE windows, or to look for abscess
Modified Duke Criteria (high-yield structure)
Major criteria
- Positive blood cultures with typical organisms from 2 separate cultures, or persistently positive cultures
- Evidence of endocardial involvement:
- Echo showing vegetation, abscess, or new partial dehiscence of prosthetic valve
- New valvular regurgitation
Minor criteria
- Predisposition (IVDU, structural heart disease)
- Fever ≥ C
- Vascular phenomena (Janeway, emboli, mycotic aneurysm, intracranial hemorrhage)
- Immunologic phenomena (Osler, Roth, GN, RF)
- Microbiologic evidence not meeting major criteria
Typical Step diagnosis rule-of-thumb:
- Definite IE = 2 major or 1 major + 3 minor or 5 minor.
Treatment: Step-Approach + Common Regimens
Principles
- Start with cultures first (unless unstable)
- Use IV bactericidal antibiotics for weeks
- Tailor to organism + susceptibility
- Consider surgery if complications or poor response
Empiric therapy (conceptual)
Empiric choices depend on:
- Native vs prosthetic valve
- Community vs healthcare-associated
- IVDU
- MRSA risk
High-yield empiric concept: cover Staph aureus (including MRSA) + strep ± enterococcus until cultures return.
Targeted therapy (board-relevant pairings)
- Viridans strep: penicillin G or ceftriaxone (± gentamicin in select cases)
- MSSA: nafcillin/oxacillin (or cefazolin)
- MRSA: vancomycin (or daptomycin for right-sided/native in some contexts)
- Enterococcus: ampicillin + ceftriaxone or ampicillin + gentamicin (resistance-dependent)
- HACEK: ceftriaxone
(Real-life regimens vary by resistance patterns and guidelines, but the Step-level “bug-to-drug” mapping above is the core.)
When Do You Need Surgery? (High-Yield Indications)
Think “Failing valve, failing antibiotics, or flying emboli.”
- Heart failure due to acute severe regurgitation (most important)
- Uncontrolled infection:
- Abscess, fistula, persistent bacteremia despite appropriate antibiotics
- Fungal IE (often surgical)
- Prevention of embolization:
- Large vegetations with recurrent emboli (especially left-sided)
- Prosthetic valve endocarditis with dehiscence or paravalvular complications
Complications You Should Be Ready to Name
- Septic emboli → stroke, splenic infarct/abscess, renal infarcts
- Mycotic aneurysms (infected arterial wall, often intracranial)
- Immune complex GN
- Perivalvular abscess → conduction abnormalities (e.g., new AV block with aortic valve IE is a red flag)
- Acute valvular insufficiency → pulmonary edema, shock
First Aid–Style High-Yield Associations (Rapid Review)
If the stem says…
- IV drug use + fever + cough/hemoptysis → tricuspid IE (often S. aureus) → septic pulmonary emboli
- Dental procedure + subacute symptoms + known murmur → viridans strep
- Prosthetic valve + fever → S. epidermidis (biofilm) until proven otherwise
- Colonoscopy/GU manipulation + subacute IE → enterococcus
- Culture-negative + exposure to farm animals → Coxiella burnetii
- Painful fingertip nodules → Osler nodes (immune)
- Painless palm/sole lesions → Janeway lesions (septic emboli)
Exam Pitfalls (Common Step Traps)
- Don’t confuse Osler (painful, immune) vs Janeway (painless, embolic).
- Right-sided IE embolizes to the lungs, not the brain.
- S. aureus is the big reason “IE can occur on normal valves.”
- TEE > TTE for prosthetic valves and detecting abscesses—Step loves this nuance.
- Get blood cultures before antibiotics unless the patient is crashing.
Quick Self-Check Questions (1-minute drill)
- IVDU with fever and multiple cavitary lung nodules: which valve/bug?
- New AV block + aortic regurg murmur + fever: what complication are you worried about?
- Dental work weeks ago + indolent fever + splinter hemorrhages: likely organism?
If you can answer those quickly, you’re in excellent shape for Step endocarditis.