Bacteremia, Septicemia & Endocarditis
🟢 Lite — Quick Review (1h–1d)
Rapid summary for last-minute revision before your exam.
Bacteremia = presence of bacteria in blood; Septicemia = clinical illness from bacteria/toxins in blood. These are not synonymous.
Key pathogens for NEET PG:
- Staphylococcus aureus — #1 cause of acute infective endocarditis (native valves, IV drug users)
- Viridans streptococci (S. mutans, S. mitis) — #1 cause of subacute bacterial endocarditis on damaged valves
- Enterococci — UTIs, biliary, GI procedures
- HACEK group (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella) — culture-negative endocarditis, slow-growing
- S. epidermidis — prosthetic valve endocarditis (early, within 60 days)
- Pseudomonas aeruginosa — IV drug users, healthcare-associated
- Culture-negative causes: Bartonella, Coxiella burnetii (Q fever), Chlamydia, Brucella
Duke Criteria (major): Positive blood cultures ×2–3 sets; echocardiogram showing vegetations. Minor: Fever >38°C, vascular phenomena, immunologic phenomena, single positive blood culture.
⚡ Exam tip: “New murmur + IV drug user” = S. aureus. “Subacute, damaged valve, oral flora” = Viridans strep.
🟡 Standard — Regular Study (2d–2mo)
Standard content for students with a few days to months.
Bacteremia vs Septicemia
| Feature | Bacteremia | Septicemia |
|---|---|---|
| Definition | Bacteria present in blood | Clinical illness from bacteria in blood |
| Symptoms | Often asymptomatic | Fever, chills, hypotension, DIC |
| Source | Often from mucosal breach | Usually from focal infection |
Acute Bacterial Endocarditis (ABE)
- Causative organisms: S. aureus (#1 overall, 40–50%), S. aureus from IV drug use (right-sided, tricuspid valve)
- Clinical: Fever, new murmur, rapid destruction of valves, systemic embolization
- Outcome: Death in days to weeks if untreated; vegetations are large and friable
- Complications: Acute heart failure (valve regurgitation), septic emboli to lungs (right-sided) or brain/kidney/spleen (left-sided), mycotic aneurysms
Subacute Bacterial Endocarditis (SBE)
- Causative organisms: Viridans streptococci (alpha-hemolytic, part of oral flora), Enterococcus faecalis, HACEK group
- Clinical: Low-grade fever, night sweats, weight loss over weeks–months; often pre-existing valvular disease (rheumatic/calcific/degenerative)
- Vegetations: Smaller, less friable than ABE
- Immune complex deposition: Osler nodes (painful, digital), Janeway lesions (painless, palmar), Roth spots (retinal hemorrhages), splenomegaly
Native Valve vs Prosthetic Valve Endocarditis
| Native Valve | Prosthetic Valve (Early <60d) | Prosthetic Valve (Late >60d) | |
|---|---|---|---|
| #1 organism | S. aureus | S. epidermidis | Viridans strep / S. aureus |
| Enterococci | Common | Less common | — |
Diagnosis
- Blood cultures: 3 sets from different sites before antibiotics; incubate 5–7 days (HACEK needs extended incubation)
- Echocardiography: TTE for native valves, TEE for prosthetic valves and aortic root
- Vegetations: Oscillating masses on valve leaflets or supporting structures
- Lab: Anemia of chronic disease, raised ESR/CRP, proteinuria (kidney involvement)
Treatment
| Organism | Antibiotic of Choice |
|---|---|
| Viridans strep | Penicillin G + Gentamicin (4–6 weeks) |
| S. aureus (MSSA) | Flucloxacillin/Nafcillin |
| S. aureus (MRSA) | Vancomycin |
| Enterococci | Ampicillin + Gentamicin |
| HACEK | Ceftriaxone or Ampicillin-Sulbactam |
Surgical indications: Acute severe valve regurgitation, uncontrolled infection (abscess, fistula), resistant organisms, recurrent emboli despite antibiotics.
🔴 Extended — Deep Study (3mo+)
Comprehensive coverage for students on a longer study timeline.
Pathophysiology of Vegetation Formation
Endothelial damage → platelet-fibrin deposition → bacterial colonization → vegetations enlarge. Damaged valves (from rheumatic heart disease, calcific degeneration, congenital lesions like bicuspid aortic valve) are prerequisite for SBE. Normal valves can be seeded in ABE/S aureus.
Right-Sided Endocarditis
- Setting: IV drug users (HIV hepatitis B/C), central venous catheters, pacemaker leads
- Tricuspid valve most commonly affected (90%)
- Clinical: Pulmonary septic emboli (pneumonia, lung abscess, septic pulmonary emboli on CT)
- Organisms: S. aureus >> Pseudomonas, Candida
- Prognosis: Better than left-sided; fatality ~10–15%
Culture-Negative Endocarditis
Causes ( mnemonic: “BOCHAPS”):
- Bartonella (50% of culture-negative)
- Coxiella burnetii (Q fever, farm animal exposure)
- HACEK organisms
- Aspergillus (fungal)
- Physical: prior antibiotic therapy (most common reason for negative culture!)
Diagnosis: Serology (Bartonella, Coxiella), PCR of blood, TEE
Infective Endocarditis in Special Populations
Rheumatic Heart Disease
- Recurrent streptococcal pharyngitis → autoimmune carditis → valvular scarring
- Mitral valve most commonly affected (stenosis > regurgitation); aortic valve second
- Patients with RHD are the classic substrate for SBE with viridans streptococci
- Jones Criteria (revised) for rheumatic fever: 2 major OR 1 major + 2 minor + evidence of preceding strep infection
Congenital Heart Disease
- VSD, PDA, bicuspid aortic valve, coarctation — all increase risk
- Cyanotic CHD has highest risk (unrepaired, Eisenmenger physiology)
Fungal Endocarditis
- Candida, Aspergillus — IV drug users, prolonged ICU stay, central lines
- Large vegetations; emboli to major vessels (e.g., large artery occlusion)
- Treatment: Amphotericin B + surgical valve replacement
Complications of Infective Endocarditis
Cardiac: Heart failure (most common cause of death), perivalvular abscess, conduction abnormalities (from septal abscesses), valve perforation or fistula
Embolic: Stroke (cerebral infarct, mycotic aneurysm rupture → SAH), splenic infarct/abscess, renal infarct, limb ischemia (septic emboli)
Immunologic: Glomerulonephritis (immune complex, often focal), Osler nodes, Janeway lesions, Roth spots, arthritis
Prevention (NVE prophylaxis — 2007 AHA guidelines)
No longer recommended for: Routine dental procedures, TEE, colonoscopy. Still recommended for:
- Prosthetic cardiac valves
- Previous infective endocarditis
- Unrepaired cyanotic CHD, repaired CHD (first 6 months)
- Cardiac transplant recipients with valve regurgitation
Regimens: Amoxicillin 2g PO 30–60 min before procedure; clindamycin 600mg if penicillin-allergic.
Key NEET PG Pearls
- S. aureus = most common cause of acute bacterial endocarditis in both native and IV drug use-associated endocarditis
- Viridans streptococci = #1 cause of subacute endocarditis on previously damaged valves
- Culture-negative endocarditis: Bartonella and Coxiella are most common causes; always ask about animal contact (cats = Bartonella henselae; farm animals = Coxiella)
- Osler nodes = painful (immunologic, immune complex); Janeway lesions = painless (vascular, septic emboli)
- Duke criteria: Need 2 major OR 1 major + 3 minor OR 5 minor for definite diagnosis
- Prosthetic valve early (<60 days) → S. epidermidis; late (>60 days) → similar to native valve
- Right-sided endocarditis + IV drug user = think S. aureus, tricuspid valve, pulmonary emboli
- Echocardiogram (TEE more sensitive than TTE) is essential for diagnosis and assessing complications
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