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PA26.{5,7} | Rheumatic Heart Disease & Infective Endocarditis — SDL Guide (Part 4)

Duke Criteria — Clinical Diagnosis of Infective Endocarditis

Infographic summarizing modified Duke criteria for infective endocarditis with major criteria, minor criteria, diagnostic combinations, and classic peripheral signs. — **Panel A:** Diagnostic classification pathway showing Definite IE, Possible IE, Rejected IE, and definite IE combinations: 2 major, 1 major + 3 minor, or 5 minor criteria.. **Panel B:** Major criteria showing positive blood cultures with typical organisms and positive echocardiogram findings including vegetation, abscess, prosthetic valve dehiscence, and new valvular regurgitation.. **Panel C:** Minor criteria showing predisposing heart condition or IV drug use, fever >=38 C, vascular phenomena, immunological phenomena, and microbiological evidence not meeting major criteria.. **Panel D:** Classic peripheral and systemic signs showing Janeway lesions, Osler nodes, Roth spots, glomerulonephritis, and arterial embolic phenomena..

The Duke criteria (modified 2000) stratify patients as definite, possible, or rejected IE using major and minor criteria.

Definite IE = 2 major, OR 1 major + 3 minor, OR 5 minor criteria

MAJOR criteria:
1. Positive blood culture: Typical organism (S. viridans, S. bovis, HACEK, S. aureus, or Enterococcus) in ≥2 separate cultures, OR persistently positive blood cultures ≥12 hours apart, OR single positive for Coxiella burnetii
2. Positive echocardiogram: Vegetation, abscess, or new partial dehiscence of prosthetic valve, OR new valvular regurgitation (worsening of pre-existing murmur is NOT sufficient)

MINOR criteria:
• Predisposing heart condition or IV drug use
• Fever ≥38°C
• Vascular phenomena (arterial emboli, septic pulmonary infarcts, mycotic aneurysm, Janeway lesions)
• Immunological phenomena (glomerulonephritis, Osler's nodes, Roth spots, positive rheumatoid factor)
• Microbiological evidence not meeting major criteria

Classic peripheral signs (vascular/immune):

Sign	Nature	Location
Janeway lesions	Non-tender, haemorrhagic macules — septic microemboli	Palms, soles
Osler's nodes	Tender, painful subcutaneous nodules — immune complex deposition	Fingertips, toe pads
Roth spots	Retinal haemorrhages with white centres	Fundus
Splinter haemorrhages	Linear haemorrhages — microemboli in nail-bed capillaries	Fingernails

Memory trick: Janeway is non-tender because it is embolic (vascular); Osler is tender because it is immune-mediated (immunological).

SELF-CHECK

A 28-year-old IV drug user presents with 3 weeks of fever, night sweats, and a new tricuspid regurgitation murmur. Blood cultures grow S. aureus in 3/3 bottles. Echo shows a 12 mm mobile vegetation on the tricuspid valve. Using modified Duke criteria, this case is classified as:

A. Possible IE — only 1 major criterion (vegetation) is present

B. Definite IE — 2 major criteria (positive blood culture + vegetation on echo)

C. Possible IE — S. aureus requires 2 separate culture draws to count

D. Definite IE — 1 major (vegetation) + 3 minor criteria are met

Reveal Answer

Answer: B. Definite IE — 2 major criteria (positive blood culture + vegetation on echo)

This patient has TWO major Duke criteria: (1) Positive blood culture — S. aureus in ≥2 separate cultures satisfies the microbiological major criterion; (2) Positive echocardiogram — vegetation on the tricuspid valve. Two major criteria = Definite IE by modified Duke criteria. IV drug use (minor criterion) and fever (minor criterion) are additional supporting evidence, but the two major criteria alone establish the diagnosis.

Complications of Infective Endocarditis

A four-panel medical diagram explains infective endocarditis complications by local cardiac destruction, septic embolization, and immune complex deposition. — **Panel A:** Cutaway left heart, mitral valve vegetation, aortic valve vegetation, friable septic embolus fragments, turbulent regurgitant flow, infected valve leaflet.. **Panel B:** Valvular regurgitation, leaflet perforation, ring abscess or perivalvular abscess, valve annulus, conduction system involvement, new heart block, aorto-cavitary fistula, pericarditis.. **Panel C:** Left-sided IE systemic emboli to brain, kidney, spleen, and coronary arteries; ischemic stroke, cerebral abscess, renal abscess, renal infarct, splenic abscess, myocardial infarction, mycotic aneurysm; right-sided IE pulmonary septic emboli and multiple lung abscesses.. **Panel D:** IgG and complement immune complexes, glomerular capillary deposition, diffuse proliferative glomerulonephritis, hematuria, proteinuria, renal impairment, acute kidney injury, Osler nodes, Roth spots, arthralgia..

IE complications are grouped by mechanism:

Cardiac complications (local destruction):
• Valvular regurgitation — the commonest acute complication; vegetation erodes or perforates the leaflet; acute severe regurgitation → acute left heart failure
• Ring abscess (perivalvular abscess) — S. aureus spreads into the valve annulus; can involve the conduction system → new heart block
• Fistula formation — e.g., aorto-cavitary fistula
• Pericarditis — haematogenous spread or direct extension

Embolic complications:
• Friable vegetations fragment → septic emboli travel in the bloodstream
• Left-sided IE → systemic emboli: brain (ischaemic stroke, cerebral abscess), kidney (renal abscess, infarct), spleen (splenic abscess), coronary arteries (myocardial infarction)
• Right-sided IE (IV drug users) → pulmonary septic emboli → multiple lung abscesses
• Mycotic aneurysm — septic embolus lodges in vessel wall → local infection → aneurysmal dilatation → rupture risk

Immune complex complications:
• Diffuse proliferative glomerulonephritis — immune complex (IgG + complement) deposition in glomeruli → haematuria, proteinuria, renal impairment; can cause acute kidney injury
• Osler's nodes, Roth spots, and arthralgia — immune complex vasculitis

Vegetations Comparison Table — The Big Picture

⚑ AI image — pending faculty review (auto-QA score 6/10; best of 3 attempts)

Five-panel comparison diagram showing the cause, size, and valve distribution of rheumatic, acute infective, subacute infective, NBTE, and Libman-Sacks vegetations. — **Panel A:** Rheumatic fever: small 1–2 mm verrucae along the line of closure; autoimmune ARF; classically mitral valve involvement.. **Panel B:** Acute infective endocarditis: large bulky friable vegetations; commonly Staphylococcus aureus or virulent organisms; destructive valve lesions.. **Panel C:** Subacute infective endocarditis: small to medium vegetations on previously damaged valve; commonly Streptococcus viridans; less destructive than acute IE.. **Panel D:** Non-bacterial thrombotic endocarditis: sterile small to medium flat pale vegetations along valve leaflet edges; associated with hypercoagulable states, malignancy, or debilitating illness.. **Panel E:** Libman-Sacks endocarditis: sterile verrucous vegetations on both sides of valve leaflets; associated with systemic lupus erythematosus..

Comparing vegetation types across conditions is a favourite exam question and essential for differential diagnosis:

Feature	Rheumatic (ARF)	Acute IE	Subacute IE	NBTE	Libman-Sacks
Cause	Autoimmune (ARF)	S. aureus, virulent organisms	S. viridans, low-virulence organisms	Hypercoagulable states, malignancy, debilitating illness	Systemic lupus erythematosus (SLE)
Size	Small (1–2 mm)	Large, bulky (cm)	Small-medium	Small-medium, flat	Small
Appearance	Warty, regular verrucae	Bulky, irregular, friable, destructive	Wart-like, less destructive	Flat, bland, sterile	Flat, may involve both surfaces
Location	Along valve closure lines (atrial surface mitral/tricuspid)	Atrial surface of AV valves; ventricular surface of semilunar valves	Same as acute IE	Along closure lines; any valve	Both atrial AND ventricular surface (distinctive); involves valve undersurface
Destruction	Minimal initially	Severe — leaflet perforation, chordal rupture	Moderate	None (sterile)	None–mild
Sterile/Infected	Sterile	Infected	Infected	Sterile	Sterile
Embolism risk	Low	High (friable)	Moderate	Moderate	Moderate
Sequelae	Chronic valve fibrosis → stenosis	Acute regurgitation, abscess, septic emboli	Subacute regurgitation, immune complications	Transient ischaemic attacks, stroke	Valvular dysfunction, IE risk

A five-panel comparison diagram shows rheumatic verrucae, acute infective endocarditis, subacute infective endocarditis, NBTE, and Libman-Sacks vegetations by size, valve location, destructiveness, and sterile versus infected status. — **Panel A:** Rheumatic verrucae: small sterile bead-like vegetations along the line of closure.. **Panel B:** Acute infective endocarditis: large infected bulky friable vegetations with destructive valve erosion.. **Panel C:** Subacute infective endocarditis: medium infected vegetations with less destruction, often on a previously abnormal valve.. **Panel D:** Nonbacterial thrombotic endocarditis: flat bland sterile thrombi along the line of closure.. **Panel E:** Libman-Sacks endocarditis: sterile vegetations on both surfaces of the valve leaflet, classically associated with SLE..

CLINICAL PEARL

The IV drug user rule: Right-sided IE (tricuspid valve) with septic pulmonary emboli is virtually pathognomonic of IV drug abuse — S. aureus is the culprit in >80% of cases. These patients do NOT usually have pre-existing valve disease. Right-sided IE carries a lower in-hospital mortality than left-sided IE because pulmonary emboli are more survivable than systemic emboli — but recidivism and repeat infection make long-term prognosis poor.

SELF-CHECK

On endomyocardial biopsy of a patient with suspected chronic active rheumatic carditis, the pathologist identifies large macrophage-derived cells with a central wavy bar of chromatin. These cells are:

A. Reed-Sternberg cells — diagnostic of Hodgkin lymphoma infiltrating the myocardium

B. Anitschkov cells (caterpillar cells) — pathognomonic of rheumatic carditis

C. Langhans giant cells — indicating granulomatous myocarditis (sarcoid/TB)

D. Foam cells — indicating lipid-laden macrophages in atherosclerotic plaque

Reveal Answer

Answer: B. Anitschkov cells (caterpillar cells) — pathognomonic of rheumatic carditis

Anitschkov cells (also called caterpillar cells or owl-eye cells) are pathognomonic for rheumatic carditis. They are modified macrophages with a distinctive nucleus where the chromatin is condensed into a central wavy bar resembling a caterpillar. They are the cellular hallmark of the Aschoff body. Reed-Sternberg cells have a 'mirror-image owl-eye' bilobed nucleus; Langhans giant cells have peripherally arranged nuclei in a horseshoe; foam cells are lipid-laden and appear vacuolated.

Putting It Together — Clinico-Pathological Correlation

A horizontal timeline diagram shows the progression from streptococcal pharyngitis to acute rheumatic fever, silent mitral valve scarring, chronic rheumatic mitral stenosis, and complications including atrial thrombus, stroke, and infective endocarditis. — **Panel A:** Phase 1 - Acute rheumatic fever: streptococcal pharyngitis, pancarditis, pericardial inflammation, myocarditis with PR prolongation, mitral endocarditis with regurgitation, Aschoff body, verrucae on valve closure line.. **Panel B:** Phase 2 - Silent scarring: recurrent streptococcal infections, repeated ARF attacks, cumulative fibrosis, thickened mitral leaflets, commissural fusion, progressive mitral stenosis.. **Panel C:** Phase 3 - Chronic RHD: fish-mouth mitral stenosis, left atrial enlargement, MacCallum plaque, pulmonary venous congestion, pulmonary hypertension, right heart failure, dyspnoea, orthopnoea, haemoptysis, atrial fibrillation.. **Panel D:** Phase 4 - Complications: atrial fibrillation, left atrial thrombus, embolic stroke, damaged valve, bacteraemia, subacute infective endocarditis due to Streptococcus viridans, Duke criteria, friable vegetations, acute regurgitation.. **Bottom ribbon:** Prevention: primary penicillin treatment for streptococcal pharyngitis and monthly benzathine penicillin secondary prophylaxis to prevent recurrent ARF and halt valve damage..

The timeline of rheumatic and endocarditic heart disease illustrates how pathology drives clinical presentation:

Phase 1 — ARF (weeks after strep pharyngitis):
• Pancarditis → pericardial friction rub + myocarditis (PR prolongation, cardiomegaly) + endocarditis (mitral regurgitation murmur)
• Aschoff bodies in myocardium; verrucae on valves
• Most patients recover fully; ~30–40% develop chronic valve disease

Phase 2 — Silent scarring (years to decades):
• Repeated strep infections → repeated ARF attacks → cumulative valve scarring
• Fibrosis + commissural fusion → progressive mitral stenosis
• No symptoms until valve area falls below ~2 cm²

Phase 3 — Chronic RHD (symptomatic mitral stenosis):
• Dyspnoea, orthopnoea, AF, haemoptysis, right heart failure
• Echocardiography: fish-mouth valve, gradient, pulmonary hypertension
• MacCallum's plaque in left atrium

Phase 4 — Complication layer:
• AF → thrombus in left atrium → stroke
• Damaged valve + bacteraemia → subacute IE (S. viridans) → Duke-criteria-positive
• IE vegetations → embolic stroke or acute regurgitation

Prevention is the key: A single course of penicillin for strep pharyngitis in Phase 1 prevents this entire cascade. Secondary prophylaxis (monthly benzathine penicillin) prevents recurrent ARF attacks and halts further valve damage — the most effective cardiovascular preventive intervention available in resource-limited settings.