Infective endocarditis Olcay ÖZVEREN, M.D.

1. Infective endocarditis Olcay ÖZVEREN, M.D.

2. Definition • Infective endocarditis is characterized bycolonization or invasion of the heart valves orthe mural endocardium by a microbe, leading tothe formation of bulky,friablevegetationscomposed of thromboticdebris and organisms, often associated withdestruction of the underlying cardiac tissues

3. A changingepidemiology: • Once a disease affecting young adults with previously well-identified (mostly rheumatic)valve disease, IE is now affecting older patients who moreoften develop IE as the result of health care-associated procedures,either in patients with no previously known valve disease or in patients with prosthetic valves. • Trials showed an increasing incidence of IE associatedwith a prosthetic valve, an increase in cases with underlying mitralvalve prolapse, and a decrease in those with underlying rheumatic heart disease. • Newer predisposing factors have emerged—valve prostheses, degenerative valve sclerosis, intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia,resulting in health care-associated IE.

4. 3–10episodes/100 000 person-years. • increaseddramaticallywithage. • Themale:female ratio is 2:1. • Positivebloodculturesrepresenting 85% of all IE. • Causativemicroorganismsaremostoftenstaphylococci, streptococci, andenterococci. • S. Aureusis the most frequent cause not only of IE but also of prostheticvalve IE. Conversely, coagulase-negativestaphylococci can also cause native valve IE. Especially S. lugdunensis, which frequently has an aggressive clinicalcourse. • Oral (formerly viridans) streptococci species such as S. sanguis, S. mitis, S. salivarius, S. mutans, andGemellamorbillorum. Microorganismsof this group are almost always susceptible to penicillin G. • Infective endocarditis with negative blood culturesbecause of prior antibiotic treatment.

5. Infective endocarditis associated withnegativebloodcultures • They are usually due to fastidious organisms such as …nutritionallyvariant streptococci …fastidious Gram-negative bacilli of the HACEK group: • (Haemophilusparainfluenzae, H. aphrophilus, H. paraphrophilus, H. influenzae, • Actinobacillusactinomycetemcomitans, • Cardiobacterium hominis, • Eikenella corrodens, • Kingella kingae,and K. denitrificans), …Brucella …fungi. …Infective endocarditis associated with constantlynegativebloodcultures: • Coxiellaburnetii, • Bartonella, • Chlamydia • Tropherymawhipplei,

6. Classification and definitions of infective endocarditis

7. Classification of infective endocarditis

8. Classification of infective endocarditis

9. Pathophysiology • The normal valve endothelium is resistant to colonization andinfectionbycirculatingbacteria. • mechanicaldisruption of theendothelium (Endothelial damage may result frommechanical lesions provoked by turbulent blood flow, electrodesor cathetersinflammation, as in rheumatic carditis, or degenerativechanges in elderly individuals, which are associated with inflammation,microulcers, andmicrothrombi) • exposure of underlyingextracellularmatrixproteins • the production of tissue factor • thedeposition of fibrin andplatelets -Nonbacterialthromboticendocarditis (NBTE)-

12. Microbial pathogens and host defences • Classical IE pathogens (S. aureus, Streptococcusspp., andEnterococcusspp.) share the ability to adhere to damaged valves, triggerlocal procoagulant activity, and nurture infected vegetations inwhich they can survive. • surface determinants that mediate adherence to host matrix moleculespresent (e.g. fibrinogen, fibronectin,platelet proteins) • trigger platelet activation. • colonization • Grampositive bacteria are resistant to complement. However, they maybe the target of platelet microbicidal proteins (PMPs), which areproduced by activated platelets and kill microbes by disturbingtheir plasma membrane. • Bacteria resistant to PMP-induced killing, • THİS is a typicalcharacteristic of IE-causingpathogens.

17. Janeway Lesions • More specific • Erythematous, blanching macules • Nonpainful • Located on palms and soles • Microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.

18. Osler’s Nodes • More specific • Painful and erythematous nodules • Located on pulp of fingers and toes • immuncomplex

19. Splinter Hemorrhages • Nonspecific • Nonblanching • Linear reddish-brown lesions found under the nail bed • Usually do NOT extend the entire length of the nail • vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small capillaries (microemboli).

20. Petechiae • Nonspecific • Often located on extremities • or mucous membranes

21. Roth Spots septic embolization, leukemia, lupus erythematosus, or pernicious anemia.

22. Imaging • Chest x-ray • Look for multiple focal infiltrates and calcification of heart valves • EKG • Rarely diagnostic • Look for evidence of ischemia, conduction delay, and arrhythmias • Echocardiography

41. Complications • Congestive heart failure • Most common complication • Main indication to surgical treatment • ~60% of IE patients • Uncontrolled infection • Persisting infection • Perivalvular extension in infective endocarditis • Systemic embolism • Brain, spleen and lungs • 30% of IE patients • May be the first symptom

42. Complications • Neurologicevents • Acuterenalfailure • Rheumaticproblems • Myocarditis

44. Cardiac conditions at highest risk of infective endocarditis for which prophylaxis is recommended when ahigh risk procedure is performed

45. Recommendations for prophylaxis of infective endocarditis

46. ACUTE RHEUMATIC FEVER

47. Definition Current Diagnosis 07 • An acute systemic immune disease that may develop after an infection with Group A beta- hemolytic Streptococcal infection of the pharynx. • This disease can affect the HEART, JOINTS, SKIN, SUBCUTANEOUS TISSUE, BRAIN, RESPIRATORY SYSTEM, VESSELS, SEROSAL MEMBRANES, TENDONS AND FASCIAL SHEATHS

48. General Consideration