Endocarditis & Cardiovascular Infections
Duke criteria, organism-by-setting, and the surgery triggers
Overview and diagnosis
Vegetations on the endocardium. Infective endocarditis is infection of the valves or endocardium that builds vegetations of platelets, fibrin, and organisms. The mitral valve is most often involved overall; IV drug users classically get right-sided tricuspid disease, which often shows up as septic pulmonary emboli. Other risk factors are prior endocarditis, prosthetic valves, structural or congenital heart disease, and intravascular devices such as dialysis catheters.
Presentation. Fever is the most common finding, joined by a new or changing regurgitant murmur, embolic and immunologic phenomena, anemia, and in subacute cases splenomegaly. New murmur plus fever plus positive cultures should trigger echo.
Three blood cultures before antibiotics. Draw 3 sets from separate sites before starting antibiotics. Endocarditis causes continuous bacteremia, so timing matters less than obtaining them first; positive cultures anchor the diagnosis and guide therapy.
- 3 blood culture setsSeparate sites, before antibiotics
- TTE firstRapid, noninvasive
- TEE if negative or prostheticMore sensitive for vegetation and abscess
- Apply Duke criteriaMajor + minor
TTE first, TEE when you need answers. Go to transesophageal echo when TTE is negative but suspicion remains high, when a prosthetic valve is present, or to look for a perivalvular abscess. TEE is far more sensitive for vegetations.
Modified Duke criteria. Definite endocarditis requires 2 major, or 1 major + 3 minor, or 5 minor criteria. The 2023 Duke-ISCVID update keeps this structure but adds PET/CT and cardiac CT findings and Coxiella burnetii serology (phase I IgG ≥1:800) or PCR as major criteria:
- Major: a typical organism in 2 separate blood cultures; echo evidence of endocardial involvement (vegetation, abscess, new valvular regurgitation).
- Minor: predisposition (heart lesion or IV drug use), fever ≥38 °C, vascular phenomena (emboli, Janeway lesions, mycotic aneurysm), immunologic phenomena (Osler nodes, Roth spots, glomerulonephritis), and a single positive culture.
Microbiology by setting
| Organism | Classic setting | Clue or next step |
|---|---|---|
| Staphylococcus aureus | Most common overall; IV drug use (tricuspid) | Acute and virulent; attacks normal valves |
| Viridans streptococci | Dental work on previously damaged valves | Subacute, smoldering course |
| Enterococci | After GU or GI procedures | Subacute |
| Staphylococcus epidermidis | Prosthetic valves, early disease (with S. aureus) | Perioperative seeding |
| Streptococcus gallolyticus (formerly S. bovis) | Colorectal cancer | Colonoscopy is mandatory |
| HACEK, Coxiella burnetii, Bartonella | Culture-negative endocarditis | Often after prior antibiotics; serology for Coxiella and Bartonella |
Acute S. aureus hits normal valves fast; subacute viridans strep smolder on previously damaged valves. Bovis in the blood, cancer in the colon: always scope for a colorectal malignancy.
Culture-negative cases most often reflect antibiotics given before cultures were drawn. Otherwise, think of the slow-growing HACEK gram-negatives (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella), Coxiella burnetii (Q fever from farm animals), and Bartonella (cats, homelessness with body lice).
Peripheral signs and complications
| Sign | Appearance | Mechanism |
|---|---|---|
| Osler nodes | Painful pads on fingers and toes ("Osler = Ouch") | Immune complexes |
| Janeway lesions | Painless macules on palms and soles | Septic microemboli |
| Roth spots | Retinal hemorrhages with pale centers | Immunologic |
| Splinter hemorrhages | Linear streaks under the nails | Nonspecific microvascular damage |
Emboli, abscess, and glomerulonephritis. Complications include septic emboli (stroke, splenic and renal infarcts, and right-sided emboli to the lungs), perivalvular abscess with conduction block, mycotic aneurysm that can rupture, and immune-complex glomerulonephritis. Heart failure from valve destruction, classically acute aortic or mitral regurgitation, is the leading cause of death.
New PR prolongation or heart block in a patient with aortic-valve endocarditis suggests a perivalvular abscess extending into the conduction system: get a TEE and a surgical opinion.
Treatment and surgery
Empiric vancomycin, then tailor. After cultures, start empiric IV vancomycin (covers MRSA, streptococci, and enterococci) for native-valve IE, then narrow once the organism is known, for example to cefazolin or an antistaphylococcal penicillin for MSSA and to penicillin G or ceftriaxone for viridans streptococci. Prosthetic-valve IE gets vancomycin + gentamicin + rifampin. Treatment is prolonged, typically 4–6 weeks of IV antibiotics, with repeat blood cultures to document clearance.
Surgery triggers.
- Valve dysfunction causing heart failure
- Uncontrolled infection or perivalvular abscess
- Persistent bacteremia despite appropriate therapy
- Large mobile vegetations with embolization
- Fungal endocarditis
- Most prosthetic-valve infections
Prosthetic valves, devices, prophylaxis, and mimics
Prosthetic timing names the bug. Early prosthetic-valve endocarditis (<1 year) is usually coagulase-negative staphylococci (Staphylococcus epidermidis) or S. aureus from perioperative seeding; late disease resembles native-valve IE. Cardiac device (pacemaker or ICD) infections generally require complete removal of the device and leads plus antibiotics.
Prophylaxis: only the highest-risk hearts. Amoxicillin 2 g, 30–60 minutes before the procedure, is reserved for a prosthetic valve, prior IE, unrepaired cyanotic congenital heart disease, repair with prosthetic material, or cardiac transplant valvulopathy. It is given before dental procedures that manipulate the gingiva or mucosa and respiratory procedures that cut mucosa, not for GI or GU procedures.
Mitral valve prolapse alone no longer warrants prophylaxis, and neither does an innocent murmur or a fully repaired defect without residual lesion; the list is short and high-risk only.
Sterile vegetations. Nonbacterial thrombotic (marantic) endocarditis is sterile and associated with advanced malignancy (mucinous adenocarcinoma) and a hypercoagulable state. Libman-Sacks endocarditis is the sterile, verrucous vegetation of SLE that sits on both sides of the valve. Both are culture-negative and can embolize.