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MICROORGANISMS RELATED TO CARDIAC INFECTIONS

MICROORGANISMS RELATED TO CARDIAC INFECTIONS. Ramlan Sadeli. CARDIAC INFECTIONS :. Infective endocarditis Myocarditis Pericarditis. INFECTIVE ENDOCARDITIS.

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MICROORGANISMS RELATED TO CARDIAC INFECTIONS

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  1. MICROORGANISMS RELATED TO CARDIAC INFECTIONS Ramlan Sadeli

  2. CARDIAC INFECTIONS : • Infective endocarditis • Myocarditis • Pericarditis

  3. INFECTIVE ENDOCARDITIS • The proliferation of microorganisms on to endothelium of the heart. The prototypic lesion at the site of infection : the vegetation; is a mass of platelets, fibrins, micro-colonies of microorganisms and scant inflammatory cells.

  4. INFECTIVE ENDOCARDITIS : • Infection most commonly involves heart valves • May also occur on the ventricular septum (on the lower pressure site) • Or on the mitral endocardium

  5. CLASSIFICATION BASE ON : • Temporal evolution of disease • Site of infections • The cause of infections • Predisposing risk factor

  6. PORTAL OF ENTRY : Community-acquired native valve Endocarditis : • Oral cavity • Skin • Upper respiratory tract

  7. Etiology : • Viridans streptococci • Staphylococci • Haemophilus • Actinobacillus • Cardiobacterium • Eikenella • Kingella

  8. PORTAL OF ENTRY : Community-acquired : • Gastrointestinal tract • Genitourinary tract Etiology : • Streptococcus • Enterococci

  9. PORTAL OF ENTRY : Nosocomial infection : • Intravascular catheter • Nosocomial wound • Urinary tract infections

  10. Etiology : • Staphylococci (coagulase-negative) • S. aureus • Gram negative bacilli • Diphtheroid • Fungi

  11. Etiology of endocarditis among injection drug users : • S. aureus • Pseudomonas aeruginosa • Candida • Bacillus • Lactobacillus • Corynebacterium

  12. 5-15% of patients with endocarditis have negative blood culture 1/3 – ½ of these cases, cultures negative because of prior antibiotic exposure The remainder of these patients are infected by fastidious organisms

  13. Pathogenesis : • The normal endothelium is resistant to infections • Direct infections by virulent organisms (S. aureus can adhere directly to intact endothelium or exposed sub-endothelium tissue) • Development of an uninfected platelet-fibrin thrombus  serves as site of bacterial attachment

  14. Diagnosis : The diagnosis of infection endocarditis is Established with certainty only when : • Vegetations obtained at cardiac surgery • At autopsy • Or from an embolus are examined histologically and microbiologically

  15. Tabel 1. The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis

  16. Bacteremic Pattern

  17. Definite infective endocarditis • Two mayor criteria • One mayor criterion and 3 minor criteria • Five minor criteria

  18. Possible infective endocarditis • One mayor and 1 minor criterion • Three minor criteria

  19. Treatment : • Since all bacteria in the vegetation must be killed, therapy for endocarditis must be bactericidal and must be given for prolonged period • Are given par-enterally • Requires precise knowledge of the susceptibility of the causative microorganisms

  20. Myocarditis Cardiac inflammation is most commonly the result of an infectious process Most commonly caused by viruses, especially coxsackie virus B

  21. Clinical manifestations : • Asymptomatic • Fulminant condition, with arrhytmia, heart failure, and death • Most often self-limited and without sequelae • Or progresses to a chronic form and to dilated cardiomyopathy • Often a history of flu-like syndrome, viral nasopharyngitis or tonsillitis

  22. Bacterial myocarditis : • Usually as a complication of endocarditis • Patients with diphtheria may develop diphtheritic myocarditis

  23. Diagnosis : • The isolation of virus from the stool, pharyngeal washing or other body fluid • Changes in specific antibody titers • Endomyocardial biopsy

  24. Myocarditis • Treatment : • Beta interferon • Bed rest • Drug for congestive heart failure arrythmia anticoagulation

  25. Myocarditis • Full recovery is usual • Fulminant cases require heart transplant

  26. Acute pericarditis : • The most common pathologic process involving pericardium • May be classified both clinically and etiologically

  27. Clinical manifestations : • Chest pain, pericardial friction rub, electrocardiographic change, pericardial effusion with cardiac tamponade and paradoxal pulse • Pain is often absent in a slowly developing tuberculosis, post-irradiation, neo-plastic, or uremic pericarditis

  28. Etiology of infective pericarditis : - Viral : • Coxsackie virus A and B • Echovirus • Mumps • Adenovirus • Hepatitis • HIV

  29. Pyogenic bacteria : • Pneumococcus • Streptococcus • Staphylococcus • Neisseria • Legionella • M. tuberculosis

  30. Fungal : • Candida • Histoplasma • Blastomyces • Coccidioides • Other infections : • Syphilitic • Protozoal • Parasitic

  31. Pericarditis • Diagnosis : Echocardiography should be performed immediately - allows assesment of pericardial thickness, pericrdial fluid and tamponade - can be used to guide emergency pericariocentesis electrocardiogram shows diffuse ST and T changes, depressed PR interval, decreased QRS voltage

  32. Laboratory diagnosis : Pericardiocenthesis : • Pericardial effusion nearly always has the physical characteristics of an exudate • Bloody fluid is commonly due to tuberculosis • Or post-cardiac injury, post myocardial infarctions, and neoplasm, and effusion of rheumatic fever

  33. Microscopic examination : • Gram-stain smear of the centrifuged sediment of clear or slightly cloudy fluid should be examined • Purulent material should be smeared directly Culture Culture perform onto a variety of specialized agar media for identification, base on microscopic examination

  34. Pericarditis • Pericardial biopsy improves the diagnostic yield • Viral or idiopathic pericarditis is self-limiting • Purulent pericarditis requires emergency surgical drainage and systemic antibiotic • Mortality is 30 %

  35. Pericarditis Tuberculous pericarditis is treated with : - a four-drug antituberculous regimen = prednison to prevent constriction - calcific form requires pericardiectomy

  36. Post streptococcal infection : Following an acute Group A streptococcal infections (e.g. sore throat), there is a latent period of 1 – 4 weeks after which rheumatic fever nephritis occasionally develops

  37. Rheumatic fever : • The most serious sequelae of hemolytic streptococcal infections • It results in damage to heart muscle and valves • Antibodies of cell membrane antigen of staphylococci cross react with the human tissue antigen • The carditis characteristically leads to thickened and deformed valve

  38. And to perivascular granulomas in the myocardium (Aschoff bodies) that are finally replace by scar tissue • Rheumatic fever has marked tendency to be reactivated by recurrent streptococcal infections • The first attack of rheumatic fever usually produce only slight cardiac damage • It is therefore important to protect such patient from recurrent beta-haemolytic Group A streptococcal infections

  39. Thank You

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