400 likes | 806 Views
MICROORGANISMS RELATED TO CARDIAC INFECTIONS. Ramlan Sadeli. CARDIAC INFECTIONS :. Infective endocarditis Myocarditis Pericarditis. INFECTIVE ENDOCARDITIS.
E N D
MICROORGANISMS RELATED TO CARDIAC INFECTIONS Ramlan Sadeli
CARDIAC INFECTIONS : • Infective endocarditis • Myocarditis • Pericarditis
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.
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
CLASSIFICATION BASE ON : • Temporal evolution of disease • Site of infections • The cause of infections • Predisposing risk factor
PORTAL OF ENTRY : Community-acquired native valve Endocarditis : • Oral cavity • Skin • Upper respiratory tract
Etiology : • Viridans streptococci • Staphylococci • Haemophilus • Actinobacillus • Cardiobacterium • Eikenella • Kingella
PORTAL OF ENTRY : Community-acquired : • Gastrointestinal tract • Genitourinary tract Etiology : • Streptococcus • Enterococci
PORTAL OF ENTRY : Nosocomial infection : • Intravascular catheter • Nosocomial wound • Urinary tract infections
Etiology : • Staphylococci (coagulase-negative) • S. aureus • Gram negative bacilli • Diphtheroid • Fungi
Etiology of endocarditis among injection drug users : • S. aureus • Pseudomonas aeruginosa • Candida • Bacillus • Lactobacillus • Corynebacterium
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
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
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
Tabel 1. The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis
Definite infective endocarditis • Two mayor criteria • One mayor criterion and 3 minor criteria • Five minor criteria
Possible infective endocarditis • One mayor and 1 minor criterion • Three minor criteria
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
Myocarditis Cardiac inflammation is most commonly the result of an infectious process Most commonly caused by viruses, especially coxsackie virus B
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
Bacterial myocarditis : • Usually as a complication of endocarditis • Patients with diphtheria may develop diphtheritic myocarditis
Diagnosis : • The isolation of virus from the stool, pharyngeal washing or other body fluid • Changes in specific antibody titers • Endomyocardial biopsy
Myocarditis • Treatment : • Beta interferon • Bed rest • Drug for congestive heart failure arrythmia anticoagulation
Myocarditis • Full recovery is usual • Fulminant cases require heart transplant
Acute pericarditis : • The most common pathologic process involving pericardium • May be classified both clinically and etiologically
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
Etiology of infective pericarditis : - Viral : • Coxsackie virus A and B • Echovirus • Mumps • Adenovirus • Hepatitis • HIV
Pyogenic bacteria : • Pneumococcus • Streptococcus • Staphylococcus • Neisseria • Legionella • M. tuberculosis
Fungal : • Candida • Histoplasma • Blastomyces • Coccidioides • Other infections : • Syphilitic • Protozoal • Parasitic
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
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
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
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 %
Pericarditis Tuberculous pericarditis is treated with : - a four-drug antituberculous regimen = prednison to prevent constriction - calcific form requires pericardiectomy
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
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
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