Q4 LONG ANSWER 10M ★ High-yield

Describe the aetiology, pathogenesis, morphology and clinical features of infective endocarditis.

Pathology · 2nd Professional — Para-Clinical

Definition

Infective endocarditis is microbial infection of the endocardial surface, characteristically of the heart valves, producing friable vegetations of fibrin, platelets, inflammatory cells and organisms.

Classification

Feature	Acute	Subacute
Organism	Highly virulent — staphylococcus aureus	Low virulence — viridans streptococci
Underlying valve	Often normal	Usually abnormal — rheumatic, congenital, prolapse
Onset	Rapid, days	Insidious, weeks to months
Course	Fulminant; destroys the valve rapidly; death in days to weeks without treatment	Indolent; less destruction
Fever	High, swinging	Low-grade
Vegetations	Large and destructive	Smaller, with more granulation tissue

Predisposing Factors and Organisms

Setting	Usual organisms
Native valve, community acquired	Viridans streptococci (Streptococcus sanguis, mutans) — from the oral cavity after dental procedures
Acute, on a normal valve	Staphylococcus aureus
Intravenous drug users	Staphylococcus aureus; affects the right side, especially the tricuspid valve, giving septic pulmonary emboli
Prosthetic valve — early (under 60 days)	Staphylococcus epidermidis (coagulase-negative)
Prosthetic valve — late	Streptococci, staphylococci
Colonic carcinoma or gastrointestinal disease	Streptococcus bovis (gallolyticus) — its isolation demands colonoscopy
Genitourinary instrumentation	Enterococci
Culture-negative (about 10%)	HACEK organisms, Coxiella (Q fever), Bartonella, Brucella, fungi; or prior antibiotics

Predisposing cardiac lesions — chronic rheumatic valve disease (still the commonest in India), mitral valve prolapse, bicuspid aortic valve, congenital heart disease, prosthetic valves, previous endocarditis
Host factors — intravenous drug use, immunosuppression, diabetes, indwelling catheters, haemodialysis

Morphology and Pathogenesis

Endothelial injury from a turbulent jet across an abnormal valve → Deposition of platelets and fibrin → sterile vegetation (nonbacterial thrombotic endocarditis) → Transient bacteraemia — from dental work, instrumentation, or skin → Organisms adhere and colonise the sterile vegetation → They multiply within it, protected from phagocytes by the fibrin → vegetation enlarges — friable, bulky, sitting on the atrial surface of atrioventricular valves and the ventricular surface of semilunar valves → Destruction, embolisation and immune complex formation

The fibrin meshwork is why endocarditis needs prolonged, high-dose, bactericidal antibiotics — organisms deep within a vegetation are metabolically inactive and inaccessible to host defences
Complications of the valve itself — perforation, chordal rupture, ring abscess, fistula, and dehiscence of a prosthesis

Clinical Features and Diagnosis

Mechanism	Features
Infection	Fever (the commonest sign), malaise, weight loss, anaemia, splenomegaly, clubbing in long-standing cases
Valve destruction	A new or changing murmur; cardiac failure
Embolic phenomena	Stroke, splenic and renal infarcts, mycotic aneurysms, janeway lesions (painless haemorrhagic macules on palms and soles)
Immune complex phenomena	OSLER nodes (painful nodules on finger pulps), ROTH spots (retinal haemorrhages with pale centres), splinter haemorrhages, glomerulonephritis

CLINICAL PEARL

Osler nodes are Ouchy (immune); Janeway lesions are painless (embolic). The mnemonic is crude but it captures a real distinction — the immune complex lesions are tender and the septic embolic ones are not. It also explains why immune phenomena appear in subacute disease, which has had time to generate antibody, and embolic phenomena dominate in acute disease.

Modified DUKE criteria — major: positive blood cultures with a typical organism (two separate sets), and echocardiographic evidence of endocardial involvement or a new regurgitant murmur. minor: predisposing lesion or drug use, fever above 38°C, vascular phenomena, immunological phenomena, and suggestive microbiological findings
Diagnosis requires 2 major, or 1 major and 3 minor, or 5 minor criteria
Three sets of blood cultures from separate sites before antibiotics — the single most important investigation, and the one most often compromised by giving antibiotics first
Transoesophageal echocardiography is far more sensitive than transthoracic, especially for prosthetic valves and abscesses

Non-infective Vegetations

Condition	Vegetation	Setting
Rheumatic	Small, warty, firm, along the line OF closure; sterile; do not embolise	Acute rheumatic fever
Infective	Large, friable, irregular; teem with organisms; embolise readily and destroy the valve	Bacteraemia on a susceptible valve
Non-bacterial thrombotic (marantic)	Small, bland, sterile, loosely attached; embolise but do not destroy	Advanced malignancy (especially mucin-secreting adenocarcinoma), DIC, debilitating illness
LIBMAN–SACKS	Small, sterile, on either OR both surfaces of the valve	Systemic lupus erythematosus; antiphospholipid syndrome

Only infective vegetations both destroy and embolise; marantic ones embolise without destroying, and rheumatic ones destroy slowly without embolising. Stating that distinction answers most questions on the topic

Applied Aspects

Consider endocarditis in any patient with fever and a heart murmur, and in unexplained fever with a prosthetic valve or a history of drug use
Treatment — prolonged (4 to 6 weeks) high-dose bactericidal intravenous antibiotics, guided by culture and sensitivity
Surgery is indicated for heart failure from valve destruction, uncontrolled infection, abscess, prosthetic valve endocarditis, fungal infection, and recurrent emboli with a large vegetation
Prophylaxis is now restricted to the highest-risk patients — prosthetic valves, previous endocarditis, and certain congenital lesions — before dental procedures involving gingival manipulation
Good dental hygiene probably matters more than antibiotic prophylaxis, since cumulative bacteraemia from chewing and brushing greatly exceeds that from occasional dental visits
Streptococcus bovis endocarditis demands colonoscopy — the association with colonic carcinoma is strong and is easily missed
Right-sided endocarditis in a drug user presents with fever and pulmonary symptoms rather than a murmur, and the chest radiograph shows multiple cavitating nodules from septic emboli
Mortality remains 15 to 30% despite treatment, and is highest with staphylococcal and prosthetic valve infection
Do not give antibiotics before taking cultures in a stable patient — it converts a treatable diagnosis into a culture-negative one
A normal echocardiogram does not exclude the diagnosis, since vegetations under 2 mm are not seen; the Duke criteria weigh clinical and microbiological evidence too
Fever settling within a week of appropriate antibiotics is the expected course; persistent fever suggests an abscess, a resistant organism or a drug reaction

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