Infective Endocarditis Flashcards
What is infectious endocarditis?
Inflammation of the endocardium, usually to the inner valves, due to infection.
What causes infective endocarditis?
Infection of the heart is caused by a variety of organisms
Infective endocarditis is initiated by microbial colonisation of natural or prosthetic heart valves, shunts and the septa
Most often bacteria – bacterial endocarditis
How is infective endocarditis classified?
Classified in 2 ways:
Acute – presents with a high fever and high toxicity
- Death if untreated in few days or weeks
Sub-acute – presents with low grade fever, weight loss and night sweats
- Death in weeks to months
Who is most at risk for infective endocarditis?
People with heart defects are at risk
Those with previous diseases:
Infective endocarditis, rheumatic heart disease
What predisposing factors increase risk of infective endocarditis? (4)
Heart valve replacement
Intravenous drug use
Periodontal disease
Poor oral hygiene
What organisms are most commonly associated with infective endocarditis? (6)
Streptococcus viridans (30-40%) Enterococci (5-18%) Other streptococci (15-25%) Staphylococcus aureus (15-40%) Coagulase-negative staphylococci (4-30%) Gram negative bacilli (2-13%)
What are the symptoms of infective endocarditis? (11)
Symptoms of endocarditis initially resemble influenza
- Febrile - fever never exceeds 39oC
- Chills
- Night sweats
- Anorexia
- Myalgia
- Arthralgia
Some patients experience neurological symptoms
- Strokes
- Intracerebral and subarachnoid haemorrhage
Peripheral symptoms include:
- Petechiae - conjunctiva (Roth spots), bucal mucosa and extremities
- Splinter and subungual haemorrhages
- Osler nodes on digits
How does colonisation on the heart valves begin?
- Turbulent flow mechanically damages the endothelium
- Damage induces the deposition of platelets and fibrin
- Induces further deposition
- Eddies form that trap circulating bacteria
- Bacteria bind to cause more damage – inflammation and complement
- Thrombotic mesh forms - Mature vegetation
Why are patients with abnormal valves at higher risk for infective endocarditis?
Abnormal valves are prone to damage
- Turbulent flow mechanically damages the endothelium
- Fibrin and platelets are deposited
- Fibrin deposits colonised by bacteria
- Bacteria are resistant to platelet antimicrobial peptides and persist
How does mature vegetation contribute to the survival of bacterial pathogens?
Mature vegetation is a protective mechanism for the bacteria
- It is an example of the biofilm mode of growth
- Bacteria growing in a biological matrix on abiotic or biotic surfaces
- Gives protection from immune system
- Gives protection from antibiotics
How do septic emboli form?
Increased turbulence can form septic emboli
- Parts break off due to shear forces
- May block blood vessels leading to stroke or allow abscess formation
How does host immunity contribute to damage?
Inflammatory responses
- IL – 1 may have a role in causing increased fibroblast proliferation and profibrotic factors
- Deposition rate increased
Complement
- Responds to immune complexes formed in response to bacterial cells
- Complexes cause glomerulonephritis – physical blockage
- Complement causes arthritis and cutaneous squelae
- Splinter haemorrhages, Osler nodes, Janeway lesions
What complications can occur from infective endocarditis?
Heart failure or severe damage - Congestive heart failure - Ruptured chordae tendineae - Perforation of valves Complications depend on side affected - Left - coronary emboli - Right - lung complications
How is infective endocarditis treated?
Highly aggressive therapy is required due to the protective effects of the mature vegetation
- High concentrations must be given
- Balance toxicity and efficacy
- Treatment is over long periods
- Surgery may be necessary
- Removal and replacement of heart valves is common
What treatment would be given for infectious endocarditis due to E. faecium?
IV Ampicillin 2g every 4 hours
IV Gentamicin 80mg twice daily
Both given over a course of 4 weeks, however 6 weeks of combination therapy is recommended in patients who had symptoms that persisted for at least 3 months before beginning therapy