I nfective Endocarditis

1. Infective Endocarditis AL-ANOUD AL-JIFRI Consultant internal medicine ,ID

2. Infective Endocarditis:Definition • A microbial infection of a cardiac valve or the endocardium caused by bacteria, fungi, or chlamydia. • Often categorized as acute or subacute based on the rapidity of the clinical course • Alternatively described by type of risk factor e.g., nosocomial, prosthetic valve, intravenous drug use - associated • Pathological findings include the presence of friable valvular vegetations containing bacteria, fibrin and inflammatory cells. • There is often valvular destruction with extension to adjacent structures. • Embolic lesions may demonstrate similar findings.

3. Epidemiology of Endocarditis • Incidence the same or slightly increased • –1.7-6.2/100,000 depending on the population • The age of subjects with endocarditis has increased over the past 60 years (30-40 to 47-69). • Among injecting drug users the incidence is as high as 150 2000/100,000 person years. • There has been a major shift in nature of underlying valvular disorders. • There has also been a change in the microbiology of cases • Increasing incidence of staphylococci. • There has been an increasing incidence of nosocomialendocarditis - both native and prosthetic valve. • There is an increased risk of IE among injecting drug users, patients on long-term hemodialysis, patients with intravenous catheters, diabetics and HIV-infected patients.

4. Risk Factors for Infective Endocarditis • Dental procedures, poor dental hygiene • viridans streptococci, nutritionally variant streptococci, HACEK • Prosthetic valves • Early: coagulase negative staphylococci, S. aureus • Late: coagulase negative staphylococci, viridans streptococci • Gastrointestinal or genitourinary procedures • enterococci or S. bovis (colon carcinoma) • Nosocomial • S. aureus (including MRSA), Gram negatives , Candida species Brouqui and Raoult, Clin Microbiol Rev, 2001

5. Risk Factors for Infective Endocarditis • HIV • S. aureus,MRSA. • Animal or farm exposure • Coxiella , Chlamydia ,Brucella. • History of homelessness, alcoholism (body lice) • Bartonella

6. Pathogenesis of IE • The development of IE is the net result of the complex interaction between the bloodstream pathogen with matrix molecules and platelets at sites of endocardial cell damage. • In addition, many of the clinical manifestations of IE origenate from the host’s immune response to the infecting microorganism. • The following sequence of events is thought to result in IE: • formation of nonbacterial thrombotic endocarditis (NBTE) on the surface of a cardiac valve or elsewhere that endothelial damage occurs • bacteremia • adherence of the bacteria in the bloodstream to NBTE • proliferation of bacteria within a vegetation. • Dissemination of infection to other tissue sites and elicitation of systemic findings.

7. Pathogenesis of IE Mucous membranes - other peripheral tissue Valvular endothelium Congenital abnormalities, turbulent blood flow Trauma - damage at tissue surface Nonbacterial thrombus, Native valvesTransient bacteremia Adherence and colonization Platelet adherence, fibrin deposition - vegetation formation Elaboration of bacterial enzymes, proteases

8. HISTORY • history of prior cardiac lesions/or rheumatic heart disease. • historical clues pointing toward a recent source of bacteremia: • indwelling intravascular catheters • intravenous drug use.

9. Epidemiological Clues in Etiological Diagnosis ofCulture-Negative Endocarditis

13. PHYSICAL EXAMINATION • cardiac examination for signs of new regurgitant murmurs or heart failure. • stigmata of endocarditis evidence of small and large emboli with special attention to the fundi, conjunctivae, skin, and digits. • Associated peripheral cutaneous or mucocutaneous lesions of IE petechiae, splinter hemorrhages, Janeway lesions, Osler's nodes, and Roth spots. • involvement of other organs • due to embolic events (eg, focal neurologic deficits, renal and splenic infarcts) or • a neurologic evaluation evidence of focal neurologic impairment. • a systemic immune reaction (eg, glomerulonephritis, arthritis). • In right-sided endocarditis, septic pulmonary infarcts may be seen.

14. Chest radiograph of a patient with tricuspid valve endocarditis due to S. aureus

15. Splinter hemorrhages in infective endocarditis

16. Roth spots

17. Osler's nodes painful, violaceous nodules found in the pulp of fingers and toes and are seen more often in subacute than acute cases of IE

18. Janeway lesions macular, blanching, nonpainful, erythematous lesions on the palms and soles

20. Modified Duke criteria for diagnosis of infective endocarditis Definite IE Pathologic criteria Microorganism: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess OR Pathologic lesions: vegetation or intracardiac abscess, confirmed by histology showing active endocarditis. Clinical criteria 2 major criteria OR 1 major and 3 minor criteria OR 5 minor criteria

21. Modified Duke criteria for diagnosis of infective endocarditis Possible IE • 1 major criterion and 1 minor criterion OR • 3 minor criteria Rejected IE • Firm alternate diagnosis for manifestations of endocarditisOR • Resolution of manifestations of endocarditis, with antibiotic therapy for four days or less OR • No pathologic evidence of infective endocarditis at surgery or autopsy after antibiotic therapy for four days or less • Does not meet criteria for possible infective endocarditis, as above

22. Modified Duke criteria for diagnosis of infective endocarditis Major criteria Positive blood cultures for IE • Typical microorganism for infective endocarditis from two separate blood cultures • Viridans streptococci • Streptococcus bovis, including nutritional variant strains • HACEK group - Haemophilusspp,. Actinobacillusactinomycetecomitants, Cardiobacteriumhominis, Eikenellaspp, and Kingellakingae. • Staphylococcus aureus • Community-acquired enterococci, in the absence of a primary focus; OR Persistently positive blood culture, defined as recovery of a microorganism consistent with IE from: • Blood cultures drawn more than 12 hours apart OR • All of three or a majority of four or more separate blood cultures, with first and last drawn at least one hour apart Single positive blood culture for Coxiellaburnetii or antiphase I IgG antibody titer >1:800*

23. Modified Duke criteria for diagnosis of infective endocarditis Evidence of endocardial involvement Positive echocardiogram for IE • TEE recommended in patients with prosthetic valves, rated at least "possible IE" by clinical criteria, or complicated IE [paravalvular abscess]; TTE as first test in other patients. • Definition of positive echocardiogram • Oscillating intracardiac mass, on valve or supporting structures, or in the path of regurgitant jets, or on implanted material, in the absence of an alternative anatomic explanation OR • Abscess OR • New partial dehiscence of prosthetic valve New valvular regurgitation Increase in or change in preexisting murmur

26. Modified Duke criteria for diagnosis of infective endocarditis Minor criteria • Predisposition - predisposing heart condition or intravenous drug use • Fever - 38.0°C (100.4°F) • Vascular phenomena - major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions. • Immunologic phenomena - glomerulonephritis, Osler's nodes, Roth spots, rheumatoid factor. • Microbiologic evidence - positive blood culture but not meeting major criterion as noted previously (excluding single positive cultures for coagulase-negative straphylococci and organisms that do not cause endocarditis) OR serologic evidence of active infection with organism consistent with IE.

27. Complications of IE can be broadly categorized as: • Cardiac • Septic • Embolic • Neurologic • Musculoskeletal • Renal • Associated with medical treatment complications in terms of their pathogenesis, which leads to different groupings: • Embolic (eg, cerebral infarct) • Local spread of infection (eg, heart valve destruction) • Metastatic infection (eg, vertebral osteomyelitis) • Immune-mediated damage (eg, glomerulonephritis)

28. Complications of IE CARDIAC COMPLICATIONS • Heart failure  • Perivalvular abscesses  • extravalvular complications  • Pericarditis, which may be suppurative or nonsuppurative, can rarely cause pain or even cardiac tamponade •   Fistulous intracardiac connections (eg, aorta-atrial or aorta-ventricular) due to extension of infection from the valve to adjacent myocardium may rarely result in large aneurysms, a pseudoaneurysm if the aortic wall is involved , or even myocardial perforation.

29. Complications of IE EMBOLIZATION  Emboli consisting of vegetation fragments can occlude or damage virtually any blood vessel, large or small, in the systemic or pulmonary arterial circulation. As a result, emboli can produce: • Stroke • Blindness • Painful ischemic or frankly gangrenous extremities • Unusual pain syndromes (eg, due to splenic or renal infarction). • Hypoxia (due to pulmonary emboli in right-sided endocarditis). • Paralysis (due to embolic infarction of either the brain or spinal cord).

30. Complications of IE NEUROLOGIC COMPLICATIONS •  Embolic stroke • Acute encephalopathy • Meningoencephalitis • Purulent or aseptic meningitis • Cerebral hemorrhage (due to stroke or a ruptured mycotic aneurysm) • Brain abscess or cerebritis • Seizures (secondary to abscess or embolic infarction)

31. Complications of IE RENAL DISEASE • Renal infarction (due to emboli). • Drug-induced acute interstitial nephritis. • Glomerulonephritis (due to deposition of immunoglobulins and complement in the glomerular membrane). • Rarely , renal abscess can occur in patients with IE.

32. Complications of IE METASTATIC ABSCESSES • Rarely, metastatic abscesses develop in the kidneys, spleen, brain or soft tissues (eg, the psoas muscle) in the setting of IE. MUSCULOSKELETAL COMPLICATIONS • Vertebral osteomyelitis is a well known but relatively rare complication of IE. • Osteomyelitis more frequently complicates S. aureusendocarditis than IE due to other microorganis

33. Complications of IE Acute septic arthritis, involving one or more joints, may be the first clue to the presence of IE in a small percentage of patients. IE should be strongly considered in selected cases of septic arthritis: • When infections spontaneously arise in joints of the axial skeleton (eg, sacroiliac, pubic, or manubriosternal joints). • When organisms with a known propensity to cause IE (eg, S. aureus, viridans streptococci or non-group A beta-hemolytic streptococci) grow from a joint aspirate, particularly in patients without a history of recent surgery, joint infection, or trauma. • When multiple joints are infected.

34. COMPLICATIONS OF MEDICAL OR SURGICAL THERAPY • Associated with prolonged parenteral antimicrobial therapy or surgery • Aminoglycoside-induced ototoxicity or nephrotoxicity • Secondary bacteremia due to central vascular lines • Mediastinitis or early postoperative prosthetic valve endocarditis • Intravenous catheter-associated phlebitis • Drug fever • Allergic or idiosyncratic reactions to various antimicrobial agents • Bleeding due to disturbances in coagulation caused by anticoagulants (in prosthetic valve endocarditis)

35. Principles of Therapy • Bactericidal antibiotics must be used. • Prolonged therapy is necessary (6 weeks). • Treatment is best started after multiple sets of blood cultures have been taken. • Urgency in the initiation of therapy is required for acute but not subacute endocarditis. • Synergistic combinations of antibiotics are used when available.

36. Echocardiographic Features That Suggest Potential Need for Surgical Intervention Vegetation • Persistent vegetation after systemic embolization. • Anterior mitral leaflet vegetation, particularly with size 10 mm. • 1 embolic events during first 2 wk of antimicrobial therapy. • Increase in vegetation size despite appropriate antimicrobial therapy. Valvular dysfunction • Acute aortic or mitral insufficiency with signs of ventricular failure. • Heart failure unresponsive to medical therapy. • Valve perforation or rupture. Perivalvular extension • Valvular dehiscence, rupture, or fistula. • New heart block. • Large abscess or extension of abscess despite appropriate antimicrobial therapy.

37. Predictors of death Several studies have attempted to identify predictors of death in patients with IE. Each patient may have one or more of the following: • Infection with S. aureus , while mortality is lower with streptococcal infection. • Heart failure. • Diabetes mellitus. • Embolic events . • Perivalvular abscess . • Larger vegetation size. • Female gender. • Contraindication to surgery. • Low serum albumin. • Persistent bacteremia. • Abnormal mental status. • Poor surgical candidacy.

38. Mimics of Infective Endocarditis • Atrial myxoma. • Marantic endocarditis. • Left atrial thrombus. • Acute rheumatic fever with carditis. • Collagen vascular disease (SLE). • Neoplasms (carcinoid).

39. Antimicrobial Prophylaxis of Endocarditis Potential Mechanisms • Bactericidal activity. • Reduce bacterial adherence. • Reduce bacterial density in the wound at the time of surgery (for prosthetic valves).

40. Prevention of Infective Endocarditis • High risk – Prosthetic valve – Complex congenital heart disease – Previous endocarditis • Moderate risk – Acquired valvular dysfunction (e.g. rheumatic valve) – Mitral valve prolapse with regurgitation • Negligible risk – Mitral valve prolapse without regurgitation – Rheumatic fever without valvular dysfunction

41. Cardiac Conditions Associated With the Highest Riskof Adverse Outcome From Endocarditis for Which ProphylaxisWith Dental Procedures Is Reasonable • Prosthetic cardiac valve or prosthetic material used for cardiac valve repair. • Previous IE. • Congenital heart disease (CHD) • Unrepaired cyanotic CHD, including palliative shunts and conduits. • Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure. • Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization). • Cardiac transplantation recipients who develop cardiac valvulopathy.

42. Dental Procedures for Which EndocarditisProphylaxis Is Reasonable • All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. • The following procedures and events do not need prophylaxis: • routine anesthetic. • injections through noninfected tissue. • taking dental radiographs . • placement of removable prosthodontic or orthodontic appliances. • adjustment of orthodontic appliances. • Placement of orthodontic brackets . • shedding of deciduous teeth. • bleeding from trauma to the lips or oral mucosa.

43. ENDOCARDITIS PROPHYLAXIS FOR DENTAL PROCEDURES

44. PARENTERAL (FOR PATIENTS UNABLE TO TAKE ORAL DRUGS)