IOD Infective Endocarditis

Question 1

Definition?

Answer 1

Infective endocarditis refers to infection of part of the endocardium, usually the endocardial surface of a
valve (but the atrium or ventricle can be affected).
It is rare; the average GP will see one case every 20 years.
However, it is important because it has a high mortality (untreated approx 100%, treated approx 10-30%).

Question 2

Causes?

Answer 2

• usually bacterial:
- Streptococci, usually S. viridans (40-50%) – weakly pathogenic. Usually originating in the mouth.
- Staphylococci eg. S. aureus (20-30%) – highly pathogenic.
S. aureus is the most common cause in iv drug users; usually affecting the tricuspid valve.
• other bacteria eg. gram negative bacteria such as E. coli.
• less commonly fungi eg. Candida, Aspergillus.
- typically immunocompromised, iv drug users and patients with indwelling venous lines.

Question 3

Pathogenesis?

Answer 3

Bacteria are delivered to the heart during an episode of bacteraemia. This may be due to an event as trivial as tooth brushing or associated with a more invasive procedure such as surgery. As a consequence of the bacteraemia, the organisms adhere to and invade the valve.

The endocardium is normally resistant to infection, so for infection to occur:
• either there must be highly pathogenic organisms (eg. S. aureus) colonising a normal valve.
• or weakly pathogenic organisms (eg. S. viridans) colonising an abnormal valve eg. prosthetic valve, mitral or aortic regurgitation, mitral valve prolapse.

Question 4

vegetations?

Answer 4

As the organisms replicate they become enmeshed within layers of platelets and fibrin on the valve surface, forming vegetations. Inflammatory cells are also present within the vegetations
microorganism causes endothelial injury on the heart valve. Also, if the valve is abnormal, there may be turbulent blood flow across the valve.

Question 5

Complications?

Answer 5

• disturbance of valve function:
• over time the underlying structure of the valve is destroyed by the infection and this results in the development of valve regurgitation.
• embolism:
• part of the vegetation may break away from the valve and form an embolus (‘septic emboli’). The clinical effect will depend on which artery the embolus occluded. The majority of emboli from vegetations enter the cerebral circulation and so present as a stroke.
• the microorganisms within the embolus may cause destruction of the arterial wall at the site where they impact leading to the formation of a mycotic aneurysm.
• formation of antigen-antibody immune complexes:
• the antigen is probably derived from the micro-organism and the antibody is produced by the body in response to it.
• immune complexes may be deposited in the glomeruli which results in the activation of complement and recruitment of inflammatory cells.
• the clinical effects depend on where the immune complexes are deposited. For example, deposition in the glomeruli may result in glomerulonephritis ie. the immune complex deposition results in damage to cells in the glomerulus with consequent disturbance in normal renal function

Question 6

Investigations?

Answer 6

Blood cultures
• at least 3 sets of blood cultures from different sites, taken a minimum of 1 hour apart and before starting antibiotics.
• these confirms the diagnosis and guides appropriate antibiotic therapy.
Echocardiography
• transoesophageal echocardiography to identify vegetations and any complications.

Question 7

Duke’s criteria?

Answer 7

major-
positive blood cultures
typical microbes consistent with IE rom 2 diff ones
taken>12 hrs apart
or 3 cultures more than 1 hr apart
echo-valvular regurgitation, abscess and vegetations
minor-
predisposing valvular or cardiac abnormality
temp >38
vasculitis
embolisms
microbiology
echo findings