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MICROORGANISMS RELATED TO CARDIAC INFECTIONS Ramlan Sadeli
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CARDIAC INFECTIONS : Infective endocarditis MyocarditisPericarditis
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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.
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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
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CLASSIFICATION BASE ON : Temporal evolution of disease Site of infections The cause of infections Predisposing risk factor
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PORTAL OF ENTRY : Community-acquired native valve Endocarditis : Oral cavity Skin Upper respiratory tract
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Etiology : - Viridans streptococci - Staphylococci - Haemophilus - Actinobacillus - Cardiobacterium - Eikenella - Kingella
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PORTAL OF ENTRY : Community-acquired : Gastrointestinal tract Genitourinary tract Etiology : StreptococcusEnterococci
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PORTAL OF ENTRY : Nosocomial infection : Intravascular catheter Nosocomial wound Urinary tract infections
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Etiology : Staphylococci (coagulase-negative) S. aureus Gram negative bacilli DiphtheroidFungi
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Etiology of endocarditis among injection drug users : S. aureus Pseudomonas aeruginosa CandidaBacillusLactobacillusCorynebacterium
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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
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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
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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
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Tabel 1. The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis Major criteria 1. Positive blood culture : - Typical microorganisms for infective endocarditis from two separate blood - Typical microorganisms for infective endocarditis from two separate blood culture culture - Persistently positive blood culture - Persistently positive blood culture - Single positive blood culture for Coxiella burnetii or phase I IgG antibody t iter - Single positive blood culture for Coxiella burnetii or phase I IgG antibody t iter of 1 : 800 of 1 : 800 Major Criteria 2. Evidence of endocardial involvement - positive echocardiogram - positive echocardiogram - new valvular regurgitation - new valvular regurgitation Minor Criteria 1. Predisposition 2. Fever 3. Vascular phenomena 4. Immunologic phenomena 5. Microbiologic evidence
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Bacteremic Pattern
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Definite infective endocarditis Two mayor criteria One mayor criterion and 3 minor criteria Five minor criteria
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Possible infective endocarditis One mayor and 1 minor criterion Three minor criteria
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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
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Myocarditis Cardiac inflammation is most commonly the result of an infectious process Cardiac inflammation is most commonly the result of an infectious process Most commonly caused by viruses, especially coxsackie virus B Most commonly caused by viruses, especially coxsackie virus B
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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
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Bacterial myocarditis : Usually as a complication of endocarditis Patients with diphtheria may develop diphtheritic myocarditis
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Diagnosis : The isolation of virus from the stool, pharyngeal washing or other body fluid Changes in specific antibody titers Endomyocardial biopsy
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Myocarditis Treatment : Beta interferon Bed rest Drug for congestive heart failure arrythmia arrythmia anticoagulation anticoagulation
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Myocarditis Full recovery is usual Fulminant cases require heart transplant
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Acute pericarditis : The most common pathologic process involving pericardium May be classified both clinically and etiologically
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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
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Etiology of infective pericarditis : - Viral : –Coxsackie virus A and B –Echovirus –Mumps –Adenovirus –Hepatitis –HIV
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- Pyogenic bacteria : –Pneumococcus –Streptococcus –Staphylococcus –Neisseria –Legionella - M. tuberculosis
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- Fungal : –Candida –Histoplasma –Blastomyces –Coccidioides Other infections : –Syphilitic –Protozoal –Parasitic
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Pericarditis Diagnosis : Echocardiography should be performed immediately - allows assesment of pericardial thickness, pericrdial fluid and tamponade fluid and tamponade - can be used to guide emergency pericariocentesis electrocardiogram shows diffuse ST and T changes, depressed PR interval, decreased QRS voltage
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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
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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 Culture perform onto a variety of specialized agar media for identification, base on microscopic examination
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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 %
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Pericarditis Tuberculous pericarditis is treated with : - a four-drug antituberculous regimen = prednison to prevent constriction - calcific form requires pericardiectomy
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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 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
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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
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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
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