Medicine chapters
Infective endocarditis
Infection of the heart valves or endocardium: who gets it, the organisms and their clues, peripheral signs, blood cultures and echo, the modified Duke criteria, antibiotic regimens, surgery and prophylaxis.
- Endocarditis needs bacteraemia plus abnormal endothelium (damaged or prosthetic valve, congenital lesion, catheter); viridans streptococci cause most subacute native-valve cases, Staph aureus causes acute disease and right-sided disease in IV drug users.
- Think of it with fever plus a murmur; take three sets of blood cultures before antibiotics, then echo (TTE, then TOE); diagnose with the modified Duke criteria (2 major, or 1 major + 3 minor, or 5 minor).
- Treat with IV bactericidal antibiotics for 4–6 weeks (e.g. penicillin + gentamicin; vancomycin for staphylococci) and refer for surgery in heart failure, abscess, uncontrolled infection or embolism from large vegetations.
On this page
Overview
Infective endocarditis (IE) is infection of the inner lining of the heart, usually a heart valve, but also septal defects, the aorta, prosthetic valves, pacemaker leads and other implanted material. The hallmark lesion is a vegetation: a mass of platelets, fibrin, organisms and inflammatory cells.
Untreated, endocarditis is almost always fatal. Even with treatment, death and complications are common, so early diagnosis matters. In Pakistan, rheumatic heart disease and late presentation make it a frequent problem.
Aetiology and pathogenesis
Two things are needed:
- Abnormal endothelium: turbulent flow from a diseased valve or a jet (VSD, PDA) damages the surface; platelets and fibrin deposit (a sterile vegetation).
- Bacteraemia: organisms in the blood stick to this deposit and multiply.
Sources of bacteraemia: poor dental hygiene and dental procedures, IV drug use, intravascular cannulae (dialysis, TPN), skin infections, GI and urinary procedures or disease, cardiac surgery and pacemakers.
Left-sided valves (mitral and aortic) are affected most often. IV drug users are the exception: tricuspid valve infection is common.
Organisms
| Organism | Setting and clues |
|---|---|
| Viridans streptococci (Strep. sanguis, mitis, mutans, oralis) | Commonest cause of subacute endocarditis on a previously damaged native valve; source is the mouth (dental disease or procedures); more common in developing countries |
| Staphylococcus aureus | Acute, destructive, rapidly fatal; IV drug users (tricuspid), intravascular catheters, diabetics, skin infections; now the commonest cause in many high-income settings; MRSA has a poor outcome |
| Coagulase-negative staphylococci (Staph. epidermidis) | Early prosthetic valve endocarditis (acquired around the time of surgery), lines and devices |
| Enterococci (E. faecalis) | Older patients after genitourinary or GI procedures or infection |
| Strep. bovis (gallolyticus) | Associated with colonic cancer or polyps: colonoscopy is essential |
| HACEK group (Haemophilus, Aggregatibacter/Actinobacillus, Cardiobacterium, Eikenella, Kingella) | Slow-growing Gram-negatives; insidious course; may be culture-negative on routine cultures |
| Fungi (Candida, Aspergillus) | IV drug users, long-term lines, immunosuppression, prosthetic valves; large vegetations; usually need surgery |
Culture-negative endocarditis
Accounts for about 5–10% of cases. Causes:
- Prior antibiotics (the commonest reason; ask carefully).
- Fastidious organisms: Coxiella burnetii (Q fever), Bartonella (cat-scratch, trench fever), Brucella (important in Pakistan), Legionella, Chlamydia, HACEK, fungi.
- Diagnose with serology, PCR of valve tissue, prolonged culture.
Non-infective endocarditis (to distinguish)
- Libman–Sacks endocarditis: sterile vegetations on both surfaces of the mitral valve in SLE/antiphospholipid syndrome.
- Marantic (non-bacterial thrombotic) endocarditis: small sterile vegetations in cancer (e.g. pancreas) and wasting states.
Risk factors
| Category | Examples |
|---|---|
| Highest risk | Prosthetic heart valve (or repair material), previous endocarditis, cyanotic congenital heart disease (unrepaired, or with shunts/conduits) |
| Other cardiac | Rheumatic heart disease, degenerative valve disease, bicuspid aortic valve, mitral valve prolapse with MR, VSD, PDA, coarctation, hypertrophic cardiomyopathy, pacemakers and ICDs |
| Non-cardiac | IV drug use, long-term IV lines and haemodialysis, poor dental hygiene, diabetes, immunosuppression, elderly |
In a young IV drug user with fever, a murmur louder on inspiration (tricuspid regurgitation) and multiple round lung shadows (septic emboli), think tricuspid endocarditis due to Staph aureus.
Presentation
Acute versus subacute
| Feature | Acute | Subacute |
|---|---|---|
| Typical organism | Staph aureus | Viridans streptococci |
| Valve | Can be normal | Usually previously damaged |
| Course | Days; high fever, toxic, rapid valve destruction | Weeks to months; low-grade fever, weight loss, malaise |
| Emboli and abscess | Common | Less common |
| Immune signs (Osler, Roth, GN) | Less time to develop | More common |
Clinical findings
The features come from four processes: infection, valve damage, emboli and immune-complex deposition.
| Feature | Approximate frequency | Mechanism |
|---|---|---|
| Fever | 90% | Infection |
| Malaise, weight loss, night sweats | 95% | Infection |
| Heart murmur (new or changing) | 90% | Valve destruction |
| Heart failure | 50% | Valve destruction |
| Haematuria (microscopic) | 70% | Glomerulonephritis or renal emboli |
| Petechiae (conjunctiva, palate, skin) | 50% | Vascular |
| Splenomegaly | 40% | Chronic infection |
| Arthralgia | 25% | Immune |
| Cerebral emboli | 20% | Embolic |
| Osler nodes | 15% | Immune |
| Clubbing | 10% | Long-standing infection |
| Splinter haemorrhages | 10% | Vascular |
| Mycotic aneurysm | 10% | Infected emboli in the vessel wall |
| Janeway lesions | 5% | Septic emboli |
| Roth spots | 5% | Immune |
Peripheral stigmata explained:
- Osler nodes: painful, tender, red nodules on the finger and toe pulps (immune-complex vasculitis).
- Janeway lesions: painless, flat red macules on the palms and soles (septic micro-emboli).
- Roth spots: retinal haemorrhages with pale centres.
- Splinter haemorrhages: thin dark lines under the nails (also seen with trauma).
- Clubbing: in long-standing subacute disease.
"Osler = Ouch." Osler nodes are painful; Janeway lesions are painless.
When to suspect IE: fever with a new regurgitant murmur; fever in a patient with a prosthetic valve, previous IE or IV drug use; unexplained embolic events (stroke, limb, spleen, kidney); new conduction block; first-time heart failure with fever; positive blood cultures with a typical organism.
Investigations
| Test | Findings |
|---|---|
| Blood cultures | At least three sets from separate venepunctures, before antibiotics (do not delay antibiotics in a very sick patient) |
| Transthoracic echo (TTE) | First imaging test; sensitivity about 60–75% for vegetations |
| Transoesophageal echo (TOE) | More sensitive (above 90%); needed for prosthetic valves, suspected root abscess, and when TTE is negative but suspicion is high |
| FBC | Normochromic normocytic anaemia, raised white cells, platelets up or down |
| ESR and CRP | Raised; CRP falls with treatment and rises with relapse |
| Urine | Microscopic haematuria, proteinuria |
| Renal function, LFTs | Raised urea/creatinine; raised alkaline phosphatase |
| Immunology | Rheumatoid factor may be positive; low complement |
| ECG | PR prolongation or heart block suggests an aortic root abscess |
| Chest X-ray | Left-sided disease: pulmonary oedema. Right-sided disease: septic emboli or lung abscesses |
| Serology | In culture-negative cases: Coxiella, Bartonella, Brucella, Legionella, Chlamydia |
| Other imaging | CT/PET-CT for prosthetic valve IE and metastatic abscesses; brain imaging for neurological signs |
Always take at least three sets of blood cultures from separate sites before antibiotics; this is the single most important test.
A normal echo does not exclude endocarditis. If suspicion stays high, repeat imaging (TOE) and cultures.
Diagnosis: modified Duke criteria
Major criteria
- Positive blood cultures:
- a typical organism in two separate cultures (viridans streptococci, Strep. bovis, HACEK, Staph aureus, or community-acquired enterococci with no other source); or
- persistently positive cultures (samples taken more than 12 hours apart, or all three, or most of four or more, with first and last at least 1 hour apart); or
- Coxiella burnetii: one positive culture or phase I IgG titre above 1:800.
- Evidence of endocardial involvement:
- echo showing a vegetation, an abscess, or a prosthetic valve that has newly started to come away (partial dehiscence); or
- new valve leak (regurgitation); a change in an old murmur is not enough.
Minor criteria
- Predisposition: predisposing heart condition or IV drug use.
- Fever of 38°C or more.
- Vascular phenomena: major arterial emboli, septic lung infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions.
- Immunological phenomena: Osler nodes, Roth spots, glomerulonephritis, positive rheumatoid factor.
- Microbiological evidence not meeting a major criterion.
Definite endocarditis
- Organism or histology from a vegetation, embolus or abscess; or
- 2 major; or 1 major + 3 minor; or 5 minor criteria.
A man with rheumatic MR has fever 38.6°C, a new louder regurgitant murmur and Roth spots. Two of three blood culture sets grow viridans streptococci. TTE shows a mitral vegetation.
Major: typical organism in two cultures (1) + vegetation on echo (1) = 2 major
Minor: predisposition, fever, immunological (Roth spots) = 3 minor
2 major criteria are enough → definite infective endocarditis
Management
Principles
- IV bactericidal antibiotics, high dose, usually for 4–6 weeks (longer for prosthetic valves).
- Choose by organism and sensitivity, with microbiology advice.
- Monitor drug levels of gentamicin and vancomycin (kidney and ear toxicity).
- Gentamicin is given with a penicillin for synergy: the penicillin damages the cell wall and lets gentamicin in.
- Watch for response within about 48 hours (fever settles, CRP falls).
Typical starting regimens (adapted from Kumar and Clark; follow local microbiology)
| Situation | Regimen (all IV) |
|---|---|
| Clinical IE, cultures awaited, staphylococci not suspected | Benzylpenicillin 1.2 g 4-hourly + gentamicin |
| Staphylococci suspected (IV drug user, recent lines or cardiac surgery, acute illness) | Vancomycin 1 g 12-hourly + gentamicin |
| Penicillin-sensitive streptococci | Benzylpenicillin + gentamicin |
| Enterococci | Amoxicillin (ampicillin) 2 g 4-hourly + gentamicin |
| Staphylococci (MSSA) | Flucloxacillin 2 g 4-hourly (± gentamicin); vancomycin if MRSA or penicillin allergy |
| Penicillin allergy | Vancomycin or teicoplanin (confirm the allergy is genuine) |
Persistent fever despite treatment: consider perivalvular abscess, drug fever, hospital-acquired infection (line, urine), pulmonary embolism, or resistant organisms. Avoid changing antibiotics without a reason; get a surgical opinion.
Surgery
Decided jointly by cardiologist and cardiac surgeon. Main indications:
- Heart failure from valve destruction (the commonest reason): e.g. severe acute AR or MR.
- Uncontrolled infection: abscess, false aneurysm, fistula, new conduction block (e.g. progressive PR lengthening), persistent positive cultures despite good antibiotics.
- Fungal or highly resistant organisms.
- Prosthetic valve endocarditis, especially early or with dehiscence.
- Prevention of embolism: large vegetations, particularly after an embolic event.
In aortic valve endocarditis, a progressively lengthening PR interval means the infection has spread into the aortic root near the AV node. This is an indication for surgery.
Complications
- Heart failure (valve destruction): the main cause of death.
- Emboli: stroke, splenic and renal infarcts, limb ischaemia; septic lung emboli in right-sided IE.
- Mycotic aneurysms (cerebral: may rupture and bleed).
- Abscesses: aortic root, myocardial, splenic, vertebral (discitis).
- Conduction block.
- Glomerulonephritis and acute kidney injury (also from antibiotic toxicity).
- Relapse.
Prevention
Antibiotic prophylaxis (current European approach; UK NICE does not advise routine prophylaxis):
- Only for highest-risk patients:
- prosthetic valves or valve repair material;
- previous infective endocarditis;
- cyanotic congenital heart disease (unrepaired or with shunts), and for 6 months after repair with prosthetic material.
- Only for dental procedures that involve the gums or tooth root (gingival or periapical manipulation) or perforate the oral mucosa.
- A single oral dose of amoxicillin before the procedure (clindamycin if allergic) is the usual choice.
- Not recommended for GI or genitourinary endoscopy, respiratory procedures, or for lesions such as mitral valve prolapse or uncomplicated valve disease.
General measures for all valve patients:
- Good dental hygiene and regular dental checks.
- Treat skin and urine infections promptly; avoid self-medication with antibiotics.
- Strict infection control for lines; prefer peripheral to central lines.
- Avoid piercing and tattoos.
A patient with mitral valve prolapse having upper GI endoscopy does not need antibiotic prophylaxis.
Prognosis
Without treatment, mortality approaches 100%. Poor outlook with Staph aureus, prosthetic valve infection, fungal infection, heart failure, abscess, and older age.
Expect: viridans streptococci as the commonest cause of subacute IE after dental work; Staph aureus in acute disease and tricuspid IE in IV drug users; Staph epidermidis in early prosthetic IE; Strep bovis needing colonoscopy; enterococci after urinary procedures; HACEK and Coxiella in culture-negative IE; Osler (painful) vs Janeway (painless), Roth spots, splinters, clubbing, haematuria and splenomegaly; three blood culture sets before antibiotics; TTE then TOE; the Duke major and minor criteria and the definite-diagnosis rule; penicillin or amoxicillin plus gentamicin and vancomycin for staphylococci for 4–6 weeks; gentamicin synergy and level monitoring; surgery for heart failure, abscess (lengthening PR), uncontrolled infection, fungi and large vegetations; prophylaxis only for high-risk patients having dental procedures, not for endoscopy.
Quick revision
- Needs damaged endothelium + bacteraemia; mitral and aortic most often; tricuspid in IV drug users.
- Viridans strep = subacute native valve; Staph aureus = acute, IVDU, lines; Staph epidermidis = early prosthetic.
- Strep bovis → colonoscopy; enterococci → GU source; culture-negative → prior antibiotics, Coxiella, Bartonella, Brucella, HACEK.
- Fever + murmur; Osler painful, Janeway painless, Roth spots, splinters, clubbing, splenomegaly, haematuria.
- Three blood culture sets before antibiotics; TTE then TOE (prosthetic valve, abscess).
- Duke definite: 2 major, 1 major + 3 minor, or 5 minor.
- IV antibiotics 4–6 weeks; monitor gentamicin and vancomycin.
- Surgery: heart failure, abscess/heart block, uncontrolled infection, fungi, prosthetic valve, large vegetations with emboli.
- Prophylaxis: highest-risk patients, dental procedures only.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What is the most common organism in subacute bacterial endocarditis?
Viridans streptococci from the mouth, usually infecting a valve already damaged by rheumatic or degenerative disease.
Why are three blood culture sets taken before antibiotics?
Bacteraemia in endocarditis is continuous but often low-grade, so several samples from separate sites raise the yield and show persistence; antibiotics given first can make cultures negative.
Why is colonoscopy needed in Streptococcus bovis endocarditis?
This organism is strongly linked with cancer and polyps of the colon, so the bowel must be examined.
Does mitral valve prolapse need antibiotic cover for endoscopy?
No. Prophylaxis is reserved for the highest-risk patients, such as those with prosthetic valves or previous endocarditis, and only for dental procedures.