Ch14: Infective Endocarditis

Preparatory Mindset

Infective endocarditis (IE) is the classic "fever + new murmur + emboli" vignette — fever and a new/changing murmur are present in ~85%, and the exam loves the Duke criteria (major: blood cultures + echocardiographic evidence; minor: predisposing heart condition, fever, vascular phenomena, immunological phenomena). The clinical skills: (1) suspect IE in any patient with fever + murmur + risk factors (prosthetic valve, previous IE, congenital heart disease, IVDU, recent dental work), (2) draw 3 blood cultures BEFORE antibiotics, (3) start empiric therapy and target the organism (S. aureus, viridans streptococci, enterococci), and (4) know surgical indications (heart failure, uncontrolled infection, emboli, fungal/Staph prosthetic-valve IE). LMCHK must-know: the HKHA antibiotic-prophylaxis indications (highest-risk patients only, for dental procedures).

Core Concepts

Definition & classification

• Infective endocarditis = infection of the endocardial surface, usually the heart valves, with vegetation formation (platelet-fibrin-bacteria matrix).
• Classification: native valve (NVE), prosthetic valve (PVE — occurs post-valve replacement; higher mortality 20–40%), right-sided (IVDU), culture-negative IE.

Epidemiology & etiology

• Organisms: Staphylococcus aureus (most common overall, acute, destructive; major cause in IVDU — right-sided), viridans streptococci (subacute, damaged/valvular disease, dental source), Enterococcus (elderly, genitourinary/GI source), Streptococcus bovis/gallolyticus (associated with colonic neoplasia — colonoscopy indicated), HACEK group (culture-negative), Candida/Aspergillus (fungal — immunocompromised, prosthetic, high mortality); culture-negative (prior antibiotics, fastidious organisms).
• Pathogenesis: endothelial injury (turbulent flow, prosthetic material) → platelet-fibrin deposition → bacteraemia seeds the vegetation → local destruction + embolisation + immune phenomena.
• Risk factors: prosthetic valve/material, previous IE, congenital heart disease (cyanotic, repaired with material), cardiac transplant with valvulopathy, IVDU, dental procedures, indwelling catheters, degenerative valve disease, immunosuppression.

Clinical manifestations

• Systemic: fever (most common), chills, night sweats, weight loss, malaise; acute (Staph — high fever, rapid deterioration) vs subacute (viridans — indolent weeks).
• Cardiac: new or changing murmur (85%) — e.g., aortic/mitral regurgitation; heart failure from valvular destruction; conduction abnormalities (myocardial abscess).
• Vascular/embolic: cerebral embolism (15–20% — MCA territory most common), splenic infarction (44% at autopsy — LUQ pain to left shoulder), renal infarction (often asymptomatic, >50% at autopsy), limb/visceral embolism, mycotic aneurysms (3–5% — aorta, cerebral, visceral).
• Immunological: Osler nodes (painful fingertip nodules), Janeway lesions (painless plantar/palmar haemorrhagic macules), splinter haemorrhages, Roth spots (retinal), glomerulonephritis, positive rheumatoid factor/hypergammaglobulinaemia (25%), circulating immune complexes (80%).

Diagnosis — Duke criteria

Major criteria:

1. Positive blood cultures: typical organisms from ≥2 separate cultures (viridans strep, S. bovis, HACEK, S. aureus, enterococci) OR persistently positive cultures; OR single culture for Coxiella burnetii.
2. Evidence of endocardial involvement: echocardiography (TTE/TEE) — vegetation, abscess, new dehiscence of prosthetic valve; new valvular regurgitation.

Minor criteria: predisposing heart condition/IVDU; fever ≥38 °C; vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, Janeway lesions); immunological phenomena (glomerulonephritis, Osler nodes, Roth spots, RF factor); microbiological evidence not meeting major criteria.

• Definite IE: 2 major, or 1 major + 3 minor, or 5 minor.
• Investigations: blood cultures ×3 before antibiotics (wait 2–7 days after antibiotics if feasible); FBC (anaemia, leukocytosis), ESR/CRP, LFTs, urine (haematuria); ECG (conduction block → abscess); TTE then TEE (TEE more sensitive for vegetations/abscess); 18F-FDG PET-CT (prosthetic-valve IE); CXR; consider cultures of urine/CSF in specific settings.

Treatment

- Viridans strep (PCN-sensitive): benzylpenicillin + gentamicin ×2 weeks, or ceftriaxone. - S. aureus (MSSA): flucloxacillin 6–12 g/day IV + gentamicin (early) — 4–6 weeks; MRSA: vancomycin (trough 15–20 μg/mL) ± rifampicin + gentamicin. - Enterococci: ampicillin + gentamicin (synergy), or vancomycin if resistant. - Culture-negative: per local protocol (often ampicillin + gentamicin ± flucloxacillin).

• Empiric (before culture): penicillin/ampicillin + antistaphylococcal agent (flucloxacillin) + gentamicin (per local protocol); vancomycin if MRSA risk or prosthetic valve (discuss with ID).
• Targeted regimens (with ID input):
• Duration: 4–6 weeks IV bactericidal therapy (native valve); prosthetic valve — longer (≥6 weeks) ± rifampicin.
• Surgical indications (high-yield): heart failure (valvular destruction), uncontrolled infection (persistent bacteraemia/fever despite appropriate antibiotics, abscess, fungal IE), prevention of emboli (recurrent emboli, large mobile vegetations >10 mm with emboli), prosthetic-valve dehiscence/Staph PVE; right-sided IE with large vegetations/ARDS.
• Complications management: heart failure (surgery), emboli (urgent surgery if recurrent), mycotic aneurysm (neurosurgery), renal failure.

High-Yield Points

• Fever + new/changing murmur (85%) + embolic/immunological phenomena → IE until proven otherwise.
• Duke criteria: major = blood cultures + echo (vegetation/abscess); minor = predisposition, fever, vascular, immunological.
• 3 blood cultures BEFORE antibiotics; TEE more sensitive than TTE.
• Organisms: S. aureus (most common, acute, IVDU right-sided), viridans strep (subacute), enterococcus (GU/GI), HACEK (culture-negative), fungal (prosthetic).
• Emboli: cerebral 15–20% (MCA), splenic 44%, renal >50% at autopsy; mycotic aneurysm 3–5%.
• Treatment: 4–6 weeks IV bactericidal; MSSA → flucloxacillin; MRSA → vancomycin.
• Surgery: heart failure, uncontrolled infection/abscess/fungal, recurrent emboli/large vegetation, PVE Staph.
• HKHA: prophylaxis only for highest-risk (prosthetic valve, previous IE, cyanotic/repaired CHD ≤6 mo, transplant valvulopathy), dental procedures only.

Topic Summary

Infective endocarditis is an endovascular infection of the valves presenting with fever, new/changing murmur, embolic and immunological phenomena; diagnosis rests on the Duke criteria (positive blood cultures + echocardiographic vegetations/abscess). S. aureus, viridans streptococci and enterococci dominate, with fungal and culture-negative forms in special hosts. Treatment is prolonged IV bactericidal antibiotics (4–6 weeks) with early surgery for heart failure, uncontrolled infection, embolic risk or prosthetic-valve infection. For LMCHK, the HKHA guidance narrows antibiotic prophylaxis to highest-risk patients for dental procedures — a frequently examined contrast with older broad-prophylaxis practice.