1. Infective endocarditis Usually involves a heart valve. Risk is much higher with a diseased valve – infection occurs with non-virulent organisms (Strep. viridans). Normal valves can be infected in septicaemia with virulent bacteria (Staph. aureus).

2. Infective endocarditis As the valves of the heart do not actually receive any blood supply of their own, defense mechanisms (such as white blood cells) cannot enter. So if an organism (such as bacteria) establishes a hold on the valves, the body cannot get rid of them. Normally, blood flows smoothly through these valves. If they have been damaged (for instance in RF) bacteria can have a chance to take hold.

3. Classification Traditionally, infective endocarditis has been clinically divided into acute and subacute (because the patients tend to live longer in subacute as opposed to acute) endocarditis. This classifies both the rate of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.

4. Etiology and pathogenesis In a healthy individual, a bacteremia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with a piece of a blood clot, the valve provides a place for the bacteria to attach themselves and an infection can be established. The bacteremia is often caused by dental procedures, such as a cleaning or extraction of a tooth.It is important that a dentist is told of any heart problems before commencing. Antibiotics are administered to patients with certain heart conditions as a precaution.

5. Clinical and pathological features Fever,i.e. fever of unknown origin (often spiking caused by septic emboli). Continuous presence of micro-organisms in the bloodstream determined by serial collection of blood cultures. Vegetations on valves on echocardiography, which sometimes can cause a new or changing heart murmur, particularly murmurs suggestive of valvular regurgitation. Vascular phenomena: (causing thromboembolic problems such as stroke in the parietal lobe of the brain or gangrene of fingers), Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles), intracranial hemorrhage. Immunologic phenomena: Glomerulo-nephritis, Osler’s nodes (painful subcutaneous lesions in the distal fingers), Roth’s spots on the retina, positive serum Rheumatoid factor.

6. Diagnosis: The most important investigation is Blood culture. >3 Blood samples from 3 different venepuncture sites.

7. Micro-organisms responsible: Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia. If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterisation, or in an IV drug user, Staphylococcus aureus is common. A third important cause of endocarditis is Enterococci.These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts.

8. Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific. Candida albicans, a yeast, is associated with IV drug users and the immunocompromised. Pseudomonas species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water. P.aeruginosa can infect a child through foot punctures, and can cause both endocarditis andseptic arthritis. Streptococcus bovis, which are part of the natural flora of the bowel, are associated with colonic malignancies.When they present as the causative agent in endocarditis, it usually calls for a concomitant colonoscopy due to worries regarding hematogenous spread of bacteria from the colon due to the neoplasm breaking down the barrier between the gut lumen and the blood vessels which drain the bowel. HACEK organisms are a group of bacteria that live on the dental gums, and can be seen with IV drug abusers who contaminate their needles with saliva. Patients may also have a history of poor dental hygiene, or pre-existing valvular disease.

9. Pathogenesis Fibrin deposits on injured endothelium. Circulating bacteria infect microthrombi. Bacterial proliferation and inflammatory infiltration/tissue destruction.

10. Infective endocarditis causes splinter hemorrhages in the nail bed:

11. Clubbing of digits:

12. Janeway lesions:

13. Janeway lesion: Janeway lesions are non-tender, small erythematous or haemorrhagic macules or nodules in the palms or soles, which are pathognomonic of infective endocarditis. The pathology is due to a type III hypersensitivity reaction. They are named after Edward.G.Janeway (1872–1917), a professor of medicine with interests in cardiology and infectious disease.

14. Roth's spots: Roth's spots are retinal hemorrhages with white or pale centers composed of coagulated fibrin. They are typically observed via fundoscopy (using an opthalmoscope to view inside the eye). They are usually caused by immune complex mediated vasculitis often resulting from bacterial endocarditis.

16. Osler's nodes: Osler's nodes are painful, red, raised lesions on the finger pulps, indicative of the heart disease subacute bacterial endocarditis. They are caused by immune complex deposition. 10–25% of endocarditis patients will have Osler's nodes. It can also be seen on the soles of the feet. They are named after Sir William Osler. It can also be seen in:  SLE  Marantic endocarditis  disseminated gonococcal infection  distal to infected arterial catheter.

18. Note: Janeway lesions are non-tender. Osler’s nodes are exquisitely tender raised reddish nodules.

19. Complications Valvular incompetence Emboli Finger clubbing Glomerulonephritis

20. Valves with infective vegetations:

21. Non-infective cardiac vegetations Systemic lupus erythematosus. Non-bacterial thrombotic endocarditis – seen in very ill people e.g. terminal cancer.

22. Libman-Sacks endocarditis