Infective Endocarditis
Medicine · Cardiology · lean revision notes
Infective Endocarditis
Infective endocarditis (IE) is a microbial infection of the endocardial surface of the heart — most often the valves — producing the characteristic lesion called a vegetation (a mass of platelets, fibrin, microorganisms and inflammatory cells). It is a favourite NEET PG topic because it ties together microbiology, the modified Duke criteria, classic peripheral signs (eponyms galore), echocardiography, antibiotic regimens, prophylaxis indications and surgical timing.
Definition & Classification
IE is defined as infection of the heart valves or mural endocardium leading to vegetation formation, valve destruction and embolic phenomena. It can also affect prosthetic material (valves, devices, leads).
Classifications you must keep ready:
| Basis | Types |
|---|---|
| Tempo | Acute (fulminant, days; usually S. aureus) vs Subacute/SBE (indolent, weeks; usually viridans streptococci) |
| Valve type | Native valve endocarditis (NVE) vs Prosthetic valve endocarditis (PVE) |
| Side | Left-sided (mitral > aortic) vs Right-sided (tricuspid — IVDU) |
| Source | Community-acquired, Healthcare-associated, IV drug use (IVDU)-related |
| Culture | Culture-positive vs Culture-negative (HACEK, Coxiella, Bartonella, prior antibiotics) |
High-yield: The most common valve involved overall is the mitral valve; in IV drug users it is the tricuspid valve; in rheumatic heart disease the mitral predominates; aortic involvement carries the worst prognosis (heart failure).
Predisposing Conditions
- Rheumatic heart disease — still the commonest substrate in India.
- Congenital heart disease — VSD, bicuspid aortic valve, PDA, tetralogy of Fallot (high-velocity jets). ASD (secundum) is classically low risk.
- Degenerative/calcific valve disease in the elderly.
- Mitral valve prolapse with regurgitation.
- Prosthetic valves and intracardiac devices.
- IV drug use, indwelling catheters, haemodialysis, immunosuppression.
The underlying mechanism is turbulent flow producing endothelial injury → deposition of platelet-fibrin (non-bacterial thrombotic endocarditis, NBTE) → transient bacteraemia seeds the sterile thrombus → bacterial proliferation within a protective fibrin meshwork inaccessible to phagocytes → mature vegetation. Because the vegetation shelters organisms from host defences, prolonged bactericidal therapy is needed rather than short courses.
High-yield: Lesions develop on the low-pressure side of a high-velocity jet (e.g., atrial surface of mitral valve in MR, ventricular surface of aortic valve in AR, and on the wall opposite a VSD jet — the "MacCallum patch" concept). This explains why regurgitant rather than stenotic lesions are higher risk.
Etiology — Organisms (must-know)
| Setting | Most likely organism(s) |
|---|---|
| Subacute NVE / dental procedures | Viridans streptococci (S. sanguinis, mutans, mitis) |
| Acute NVE, IVDU, healthcare | Staphylococcus aureus (commonest overall in developed-world data) |
| Colon cancer / GI lesion association | Streptococcus gallolyticus (S. bovis) → colonoscopy mandatory |
| Enterococci | GU instrumentation, elderly men |
| Early PVE (<60 days / <12 months) | Staphylococcus epidermidis (coagulase-negative staph) |
| Late PVE (>12 months) | Resembles NVE — viridans strep, S. aureus |
| Culture-negative | HACEK, Coxiella burnetii (Q fever), Bartonella, Brucella, Tropheryma whipplei |
| Marantic/NBTE | Malignancy, SLE (Libman–Sacks) — sterile |
High-yield: Streptococcus gallolyticus (bovis) endocarditis → look for colorectal carcinoma. HACEK = Haemophilus/Aggregatibacter, Actinobacillus, Cardiobacterium, Eikenella, Kingella — fastidious Gram-negatives, classic cause of "culture-negative" IE needing prolonged incubation.
Mnemonic for HACEK organisms: "HACEK" itself; remember they are slow-growing Gram-negative bacilli that respond to ceftriaxone.
Clinical Features
Fever (≈90%) plus a new or changing murmur is the classic combination. Subacute disease presents with constitutional symptoms — low-grade fever, weight loss, night sweats, anaemia of chronic disease, fatigue, splenomegaly.
Peripheral (immunological & embolic) signs — eponym goldmine:
| Sign | Description | Mechanism |
|---|---|---|
| Osler nodes | Painful (Ouch!), violaceous nodules on finger/toe pulps | Immune complex (vasculitis) |
| Janeway lesions | Painless, flat, erythematous macules on palms/soles | Septic emboli |
| Roth spots | Retinal haemorrhages with pale/white centre | Immune complex |
| Splinter haemorrhages | Linear subungual streaks | Microemboli/vasculitis |
| Petechiae | Conjunctiva, palate, skin | Microemboli — commonest sign |
| Clubbing | In long-standing subacute IE | Chronic |
High-yield distinction: Osler = Ouch (painful, immune), Janeway = Junk/painless (septic emboli). This single dichotomy is among the most repeated NEET PG facts.
Complications-driven presentations: heart failure (valve destruction — leading cause of death), systemic emboli (stroke, splenic/renal infarcts), mycotic aneurysm, glomerulonephritis (immune-complex), conduction block (aortic root abscess → prolonging PR interval).
Right-sided IE (IVDU) behaves differently: the patient presents with fever, cough, pleuritic chest pain and multiple septic pulmonary emboli (cannon-ball or cavitating nodules on chest X-ray) rather than peripheral stigmata, because emboli travel to the lungs, not the systemic circulation. Murmur of tricuspid regurgitation may be soft or absent. Prognosis of isolated right-sided S. aureus IE is generally better than left-sided disease.
Diagnosis — Modified Duke Criteria
Diagnosis hinges on the Modified Duke Criteria. Definite IE = 2 major, OR 1 major + 3 minor, OR 5 minor. Possible IE = 1 major + 1 minor, OR 3 minor.
MAJOR criteria (2):
- Positive blood cultures —
- Typical organism from 2 separate cultures (viridans strep, S. gallolyticus, HACEK, community-acquired S. aureus, enterococci without a focus), OR
- Persistently positive cultures (≥2 drawn >12 h apart, or 3/3 or majority of ≥4), OR
- Single positive culture for Coxiella burnetii or phase-I IgG titre >1:800.
- Evidence of endocardial involvement —
- Echocardiography: vegetation, abscess, new partial dehiscence of prosthetic valve, OR
- New valvular regurgitation (worsening of existing murmur not sufficient).
MINOR criteria (5):
- Predisposing heart condition or IV drug use
- Fever ≥ 38°C (100.4°F)
- Vascular phenomena — arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial/conjunctival haemorrhage, Janeway lesions
- Immunological phenomena — glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
- Microbiological evidence not meeting major criteria
Mnemonic (minor): "FEVER from PVIIM" — or simply Predisposition, Fever, Vascular, Immunologic, Microbiologic (PFVIM).
High-yield: The 2023 Duke-ISCVID update added intracardiac device involvement, PET/CT (¹⁸F-FDG) and CT findings as criteria, and broadened "typical organisms" — but for NEET PG the Modified Duke (2000) version above is what is examined.
Investigations — stepwise approach
Three sets of blood cultures from separate venepuncture sites, before antibiotics → Echocardiography (TTE first, TEE if needed) → CBC/ESR/CRP, RF, urinalysis → ECG (watch PR prolongation) → imaging for emboli.
| Test | Role / Pearl |
|---|---|
| Blood culture | Investigation that establishes microbiology; 3 sets over time before antibiotics |
| TTE (transthoracic echo) | First-line; sensitivity ~60–70% for vegetations; good for tricuspid |
| TEE (transoesophageal echo) | Investigation of choice for sensitivity (~90–95%); mandatory for prosthetic valves, abscess, negative TTE with high suspicion |
| ECG | New AV block suggests aortic root/annular abscess |
| ESR/CRP, RF, complement (low C3) | Support immunological activity |
| Urinalysis | Haematuria/RBC casts → glomerulonephritis |
| ¹⁸F-FDG PET/CT | Useful in PVE and device IE (newer criterion) |
High-yield: TEE detects vegetations <5 mm and abscesses far better than TTE — it is the investigation of choice for prosthetic valve endocarditis and when complications are suspected. TTE remains the initial test.
Management — Drug of Choice
Principles: prolonged (4–6 weeks) parenteral, bactericidal antibiotics, ideally culture-guided. Start empirical therapy after cultures in unstable patients.
Empirical therapy:
- Native valve (subacute/stable): Ampicillin + (flu)cloxacillin + gentamicin, or vancomycin + gentamicin if MRSA risk.
- Prosthetic valve: Vancomycin + gentamicin + rifampicin (rifampicin for biofilm/foreign material).
Organism-directed regimens:
| Organism | Drug of choice |
|---|---|
| Penicillin-susceptible viridans strep | Penicillin G or ceftriaxone × 4 weeks (±gentamicin × 2 wk to shorten) |
| MSSA (native) | Cloxacillin/Nafcillin/Flucloxacillin |
| MRSA | Vancomycin (± daptomycin) |
| Enterococci | Ampicillin + gentamicin (or ampicillin + ceftriaxone if HLAR) |
| HACEK | Ceftriaxone |
| Prosthetic valve staph | Vancomycin + rifampicin + gentamicin |
| Coxiella (Q fever) | Doxycycline + hydroxychloroquine (prolonged) |
High-yield: Rifampicin is added specifically in prosthetic valve endocarditis because it penetrates biofilm on foreign material. Gentamicin provides synergy in enterococcal and streptococcal IE.
Surgical indications (≈ when antibiotics alone fail)
- Heart failure from valve dysfunction (commonest indication).
- Uncontrolled infection — abscess, persistent bacteraemia despite appropriate antibiotics, fungal/resistant organisms.
- Prevention of embolism — large vegetation >10 mm with prior embolic event, or >15 mm mobile vegetation.
- Early prosthetic valve endocarditis, valve dehiscence, fistula.
High-yield: Vegetation >10 mm + an embolic episode, or >15 mm, on the mitral/aortic valve → consider early surgery. Congestive heart failure is the single most important indication and the leading cause of death in IE.
Antibiotic Prophylaxis (AHA/ESC)
Prophylaxis is now markedly restricted. It is given only to the highest-risk cardiac conditions undergoing high-risk procedures.
Cardiac conditions warranting prophylaxis:
- Prosthetic heart valve or prosthetic material used for valve repair.
- Previous infective endocarditis.
- Unrepaired cyanotic congenital heart disease; repaired CHD with residual defect near prosthetic material; repaired CHD with prosthetic material in first 6 months.
- Cardiac transplant recipients with valvulopathy.
Procedures needing prophylaxis: dental procedures involving gingival/periapical region or perforation of oral mucosa. Routine respiratory procedures only if incision of mucosa. GI/GU procedures no longer require routine prophylaxis.
Regimen: Amoxicillin 2 g orally, 30–60 minutes before the procedure (paediatric 50 mg/kg). If penicillin-allergic: clindamycin (historically) or azithromycin/cephalexin; if unable to take oral: ampicillin/ceftriaxone IV.
High-yield: Mitral valve prolapse without regurgitation, ASD (secundum), isolated repaired ASD/VSD/PDA after 6 months, and CABG do NOT need prophylaxis. Prophylaxis is not given for routine GI/GU procedures.
Complications
- Cardiac: heart failure (leading cause of death), valve perforation/rupture, perivalvular/aortic root abscess (→ new AV block), fistula, pericarditis.
- Embolic: stroke, splenic/renal/coronary infarction, mycotic aneurysm, septic pulmonary emboli (right-sided IE).
- Renal: immune-complex glomerulonephritis, infarction.
- Neurological: embolic stroke, cerebral abscess, intracranial haemorrhage from mycotic aneurysm.
- Metastatic infection / persistent sepsis.
Key Differentials
| Condition | Distinguishing feature |
|---|---|
| Rheumatic fever (acute) | Jones criteria, migratory polyarthritis, recent strep; no vegetations |
| Non-bacterial thrombotic endocarditis (NBTE/marantic) | Malignancy/DIC; sterile vegetations; negative cultures |
| Libman–Sacks endocarditis | SLE; verrucous sterile vegetations on both surfaces of valve |
| Atrial myxoma | Constitutional symptoms + embolism + "tumour plop"; echo shows pedunculated LA mass |
| Antiphospholipid syndrome | Valve thickening, thrombosis, negative cultures |
| PUO of other cause | No vegetations, negative Duke criteria |
High-yield: Libman–Sacks (SLE) vegetations are sterile, on both surfaces of the valve and at commissures; marantic (NBTE) vegetations are sterile and associated with adenocarcinoma/DIC. Both are culture-negative — distinguishing them from infective IE is a classic exam trap.
Recently asked / exam angle
- Single-best-answer staples: valve most involved in IVDU (tricuspid); organism after dental procedure (viridans strep); organism in early PVE (S. epidermidis); painful pulp nodule (Osler node, immune); painless palmar macule (Janeway, embolic).
- Duke criteria: number needed for "definite IE" (2 major / 1 major + 3 minor / 5 minor); which echo finding is a major criterion; which peripheral sign is vascular (minor) vs immunological (minor).
- Microbiology link: S. gallolyticus/bovis → colonoscopy for colorectal cancer; HACEK as cause of culture-negative IE.
- Echo: TTE = initial; TEE = most sensitive / investigation of choice especially in prosthetic valves and abscess.
- Prophylaxis: amoxicillin 2 g before high-risk dental work; which lesions need it (prosthetic valve, prior IE, cyanotic CHD) and which do not (MVP without MR, secundum ASD).
- Surgery: vegetation size cut-offs (>10 mm with embolism, >15 mm); CHF as prime indication.
- Drug-of-choice matches: MSSA → cloxacillin; MRSA → vancomycin; HACEK → ceftriaxone; PVE adds rifampicin.
- ECG clue: new PR prolongation / AV block → aortic root abscess → surgery.
Rapid revision
- Vegetation = platelets + fibrin + organisms; substrate is turbulent flow → NBTE → bacteraemia seeding.
- Commonest valve overall = mitral; IVDU = tricuspid; worst prognosis = aortic.
- Acute IE = S. aureus; subacute = viridans strep; early PVE = S. epidermidis.
- S. gallolyticus (bovis) IE → screen for colorectal carcinoma.
- Osler = painful immune; Janeway = painless embolic; Roth spots = retinal pale-centred haemorrhage.
- Definite IE = 2 major / 1 major + 3 minor / 5 minor (Modified Duke).
- Major Duke = positive blood cultures + echo evidence/new regurgitation.
- 3 sets of blood cultures before antibiotics; TTE first, TEE = most sensitive / investigation of choice.
- New AV block = aortic root abscess → surgery.
- PVE empirical therapy = vancomycin + gentamicin + rifampicin (rifampicin penetrates biofilm).
- Surgery indications: CHF (commonest), uncontrolled infection, vegetation >10 mm with embolus or >15 mm.
- Prophylaxis = amoxicillin 2 g, 30–60 min pre-procedure, only for highest-risk hearts (prosthetic valve, prior IE, cyanotic CHD); NOT for routine GI/GU procedures, MVP without MR, or secundum ASD.