Infective Endocarditis

Question 1

What are some signs for infective endocarditis?

Answer 1

Peripheral stigmata: Janeway lesions non-tender macular/papular lesions), splinter haemorrhages, Osler nodes (raised, tender lesions)

Fundoscopy: Roth spots

Cardiovascular examination: new/ changing murmur

Question 2

What are some risk factors for infective endocarditis

Answer 2

Congenital heart disease: rheumatic heart disease, valvular incompetence (requiring prosthetic valve replacement)

Needlestick contact: IVDU, dental surgery, blood transfusions, tattoo, healthcare occupation

Immunocompromised

Question 3

Criteria for diagnosing infective endocarditis

Answer 3

2 major criteria + 1 minor
1 major + 3 minor
5 major

Major criteria:

• Endocardial involvement - vegetation or abscess formation (commonly on the tricuspid valve)
• 2 x positive blood cultures
• Exception: single positive culture for Coxiella burnetti

Minor criteria:

• Fever >38degrees
• Positive culture but insufficient
• Immunologic phenomenon: peripheral stigmata, rheumatoid factor, glomerulonephritis
• Risk factors
• Vascular findings: Janeway lesions

Question 4

Common causative agents for infective endocarditis

Answer 4

Staph aureus
Strep viridans (pre-existing valvular damage)
Staph epidermis (esp with prosthetic valve - biofilm)
HACEK organisms - haemophilus, aggregatibacter, cardiobacterium, eikenella, kingella
Coxiella burnetti

Question 5

Pathophysiology of infective endocarditis

Answer 5

General gist: Cardiovascular risk factors + bacteremia
+/- Virulence factors: enzymes, toxins and other proteins that enable evasion of host defences and also enable spread

Endothelial injury –> fibrin and platelet aggregation –> vegetations form because bacteria evades host immune defences –> bacteria continues to colonise + grow with the fibrin cap & leukocytosis –> neutrophils release enzymes that lead to friable vegetations

Question 6

Complications of infective endocarditis

Answer 6

acute - septic shower +/- Pulmonary emboli

Cardiovascular: valvular incompetence and/or dysfunction, electrical conductivity disrupted, mycotic aneurysm (infection of the myocardium causing compromised integrity of the wall),

Septic: neuro/kidney/lungs/spleen –> infarction, haemorrhage, metastatic abscess

Immune response: glomerulonephritis and acute renal failure (deposition of immunoglobulins and complement in the glomerular membrane)

Question 7

Virulence factors of Staph Au

Answer 7

Enzymes, toxins, other factors - evade host immune defences:

1. Hyaluronidase - breaks down hyaluronic acid to enable spread
2. Coagulase - clots plasma, coats bacterial wall to avoid phagocytosis
3. Protein A - surface of Staph Au; binds to Fc region of immunoglobulins and therefore prevents phagocytosis and antibody mediated response

Question 8

Staph Au may not respond to empirical treatment. Explain why and list the features for different population groups to consider.

Answer 8

Staph au can be community acquired and hospital acquired; their resistance therefore changes due to exposure of antibiotics.

Community acquired Staph Au:

• Population group: young patients, ATSI, immunocompromised, aged care residents, IVDU
• Susceptible: Ciprofloxacin, trimethoprim, sulfamethoxazole
• Associated clinical picture: skin infections

Hospital acquired Staph Au

• Population group: old, diabetics, dialysis, prolonged hospitalisation
• multi-bug resistant; susceptible: trimethoprim and sulphamethoxazole
• Associated clinical picture: pneumonia, UTI

Question 9

Management - Antibiotics

Answer 9

‘Big Friendly Giant’ - B.F.G.

1. Benzylpenicillin
2. Flucloxacillin
3. Gentamicin (remember to measure your baseline renal function)

Targetted:
MSSA: Vancomycin
MRSA: flucloxacillin