Infective Endocarditis
A board-focused walkthrough of infective endocarditis from NBTE-to-vegetation pathogenesis through organism-by-setting microbiology, modified Duke diagnosis (2 major / 1 major + 3 minor / 5 minor), and next-best-step management, anchored by classic vignette buzzwords (Carvallo sign, FROM JANE stigmata, new AV block = aortic-root abscess). It drills the decisions boards test: cultures-then-empiric-vancomycin, TTE to TEE, and surgical indications.
Infective endocarditis (IE) is infection of the endocardial surface, almost always a heart valve. Pathogenesis: turbulent flow, a catheter, or degenerative change damages endothelium, forming a sterile platelet-fibrin thrombus (nonbacterial thrombotic endocarditis, NBTE). Transient bacteremia then seeds this nidus, creating an infected vegetation. Left-sided disease predominates (mitral > aortic) except in IV drug use, where the tricuspid valve is struck. Predisposing substrates include rheumatic and degenerative valves, mitral valve prolapse with regurgitation, bicuspid aortic valve, prosthetic valves, and congenital shunts (VSD, PDA).
Course splits into acute (virulent _Staphylococcus aureus_ on a normal valve; rapid destruction over days) and subacute (low-virulence viridans streptococci on an abnormal valve; indolent over weeks). Ongoing bacteremia plus immune-complex deposition drives the peripheral stigmata and glomerulonephritis. The leading cause of death and the leading indication for surgery are valve destruction causing heart failure, followed by embolic and perivalvular complications.
- Most common organism overall (developed world): _Staphylococcus aureus_ — also #1 in IV drug use and acute IE.
- Subacute IE on a damaged native valve: viridans streptococci (e.g., _S. sanguinis, S. mutans_) after dental work; adhere via dextran.
- Prosthetic valve <1 yr (early): coagulase-negative staph (_S. epidermidis_); late (>1 yr) resembles native-valve IE.
- _Streptococcus gallolyticus_ (bovis) IE → colonoscopy to hunt for colon cancer.
- Enterococcus after GU/GI instrumentation (older men).
- Culture-negative IE: prior antibiotics or fastidious organisms — HACEK (_Haemophilus/Aggregatibacter, Cardiobacterium, Eikenella, Kingella_), _Coxiella_, _Bartonella_.
- IV drug use → right-sided (tricuspid) IE → septic pulmonary emboli; often a previously normal valve.
- Modified Duke criteria — definite IE = 2 major, 1 major + 3 minor, or 5 minor. Major = typical organism in 2 separate blood cultures or echo evidence (vegetation, abscess, or new valvular regurgitation). Draw ≥3 culture sets from separate sites before antibiotics.
- New AV block / prolonged PR on ECG → perivalvular (aortic-root) abscess — a surgical sign.
- Sterile (no-organism) vegetations: marantic/NBTE (malignancy) and Libman-Sacks (SLE).
Organisms by clinical setting
| Setting / clue | Organism | Board pearl |
|---|---|---|
| Dental work, damaged native valve, subacute | Viridans streptococci | Adhere via dextran; indolent |
| Acute on normal valve; IV drug use | _Staphylococcus aureus_ | Most common overall; tricuspid in IVDU |
| Prosthetic valve <1 yr | Coagulase-neg staph (_S. epidermidis_) | Biofilm on hardware |
| Colon cancer / GI source | _Strep gallolyticus_ (bovis) | Do colonoscopy |
| GU/GI instrumentation, elderly men | Enterococci | Ampicillin + gentamicin |
| Culture-negative | HACEK, _Coxiella_, _Bartonella_ | Fastidious/gram-neg; often prior antibiotics |
| Marantic / Libman-Sacks | Sterile — no organism | Malignancy / SLE |
A 29-year-old who injects heroin has 5 days of fever, chills, and pleuritic chest pain. Exam: T 39.2°C and a holosystolic murmur at the left lower sternal border that increases with inspiration. Chest CT shows multiple peripheral nodular and cavitary lesions.
- Diagnosis: right-sided (tricuspid) infective endocarditis, most likely _S. aureus_, with septic pulmonary emboli.
- Murmur clue: inspiration-augmented regurgitant murmur = Carvallo sign = tricuspid regurgitation.
- Next best step: obtain ≥3 sets of blood cultures from separate sites, then start empiric vancomycin; get echocardiography (TTE first, TEE if negative, prosthetic, or complication suspected).
- Right-sided IE often lacks peripheral stigmata — Osler/Janeway/Roth phenomena are embolic/immune features of left-sided disease reaching the systemic circulation.
FROM JANE captures the classic peripheral findings:
- F — Fever
- R — Roth spots (retinal hemorrhages with pale/white centers)
- O — Osler nodes (painful, pads of fingers/toes)
- M — Murmur (new or changing regurgitant murmur)
- J — Janeway lesions (painless, palms/soles)
- A — Anemia (of chronic disease)
- N — Nail-bed splinter hemorrhages
- E — Emboli (septic — stroke, splenic/renal infarct, mycotic aneurysm)
Discriminator: Osler = Ouch (tender, immune-complex mediated); Janeway = painless (septic microemboli).
Peripheral lesions compared
| Lesion | Location | Painful? | Mechanism |
|---|---|---|---|
| Osler nodes | Pads of fingers/toes | Painful ("Ouch") | Immune complex |
| Janeway lesions | Palms / soles | Painless | Septic microemboli |
| Roth spots | Retina | — | Immune-mediated hemorrhage |
| Splinter hemorrhages | Nail beds | Painless | Microemboli |
A 62-year-old with a bioprosthetic aortic valve is 10 days into therapy for viridans-strep endocarditis when he becomes bradycardic; telemetry shows a new first-degree AV block progressing to complete heart block. TTE is unremarkable.
- Interpretation: new conduction delay signals infection burrowing into the aortic root / perivalvular tissue → perivalvular abscess — the aortic annulus abuts the AV node and His bundle.
- Next best step: transesophageal echocardiography (TEE) — far more sensitive than TTE for abscess and prosthetic-valve vegetations.
- Management: a perivalvular abscess is an indication for surgery, not antibiotics alone.
- Other surgical indications: heart failure from valve destruction (most common), persistent bacteremia despite appropriate therapy, fungal or resistant organisms, and large mobile vegetations (>10 mm) with recurrent emboli.
Management & prophylaxis
Empiric therapy after cultures: vancomycin (covers MRSA, streptococci, and enterococci); add gentamicin ± rifampin for prosthetic valves. Then narrow: MSSA → nafcillin/oxacillin or cefazolin; MRSA → vancomycin; viridans strep → penicillin or ceftriaxone; enterococcus → ampicillin + gentamicin (or ampicillin + ceftriaxone); prosthetic MRSA → vancomycin + rifampin + gentamicin. Treat 4–6 weeks IV. Operate for heart failure, perivalvular abscess/heart block, persistent infection, fungal/resistant organisms, or large vegetations with recurrent emboli.
Prophylaxis is reserved for the highest-risk hearts only: prosthetic valve or prosthetic repair material, prior IE, unrepaired cyanotic congenital disease (or repaired with a residual defect), and cardiac-transplant valvulopathy — AND a dental procedure manipulating gingiva/periapical tissue or perforating oral mucosa (or infected respiratory/skin procedures). Give amoxicillin 2 g PO 30–60 min before; penicillin-allergic: cephalexin, azithromycin, or doxycycline. Mitral valve prolapse is no longer an indication, and routine GI/GU prophylaxis is not recommended.
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