Infective endocarditis
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Definition – Infective endocarditis is a microbial infection of the heart valves or mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissue
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Infective endocarditis is classified on clinical grounds into acute and subacute forms indicating the severity of disease which depends upon the virulence of infecting organism
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Acute infective endocarditis-
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Infection of previously normal heart valve by highly virulent organism (staphylococcus aureus) that rapidly produces necrotizing and destructive lesions
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Death ensue with in days to weeks despite appropriate treatment with antibiotics and surgery
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Sub acute infective endocarditis
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Infection by organisms of lower virulence (Streptococci viridans) that causes insidious infections of deformed valves with over all less destruction
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Disease has course of weeks to months and cure can be achieved with antibiotics
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Etiopathogenesis
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Organisms causing are
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50% to 60% of cases affecting previously damaged or otherwise abnormal valves – Streptococcus viridans (normal component of oral cavity flora)
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20% to 30% of cases affecting healthy or deformed valves – Staphylococus aureus
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IE in IV drug abusers – Staphylococcus aureus
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Prosthetic valve endocarditis is caused most commonly by – Coagulase negative staphylococci (Staphylococcus epidermidis)
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Other bacterial causes include Enterococci and HACEK group
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H – Haemophilus
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A- Actinobacillus
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C – Cardiobacterium
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E – Eikenella
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K – Kingella
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Other agents causing endocarditis include – Gram negative bacilli and fungi
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In 10% of cases – no organism is identified (“Culture negative” endocarditis)
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Causes for the culture negative endocarditis are
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Prior antibiotic therapy
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Difficulty in isolating the offending agent
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Organism is deeply embedded in enlarged vegetation that it cannot be released into blood
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Predisposing factors
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3 main types of predisposing factors leading to bacterial endocarditis are
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Conditions that causes seeding of microorganisms into the blood (Bacteremia or Fungemia)
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Underlying heart disease
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Impaired host defenses
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Source of infection may be
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Periodontal infections and dental procedures
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Contaminated needle shared by IV drug abusers
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Infections of genitourinary tract during procedures like catheterization, cystoscopy, and obstetrical procedures during normal delivery or abortions
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Infections and surgeries of bowel and biliary tract
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Skin infections like boils, carbuncles and abscesses
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Respiratory tract infections
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Cardiac catheterization and surgery for valve replacement
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Commonly associated underlying heart diseases are
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Chronic rheumatic valvular disease (50% of cases)
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Congenital heart diseases (20% of cases) like
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VSD, PDA, Sub aortic stenosis, pulmonary stenosis, bicuspid aortic valve and coarctation of aorta
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Other causes are
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Syphilitic valvular disease, atherosclerotic valvular disease, floppy mitral valve, prosthetic heart valves
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Impaired host defenses
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Impaired specific immunity in lymphomas
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Leukemias
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Cytotoxic therapy for cancer patients and transplant patients
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Deficient functions of neutrophils and macrophages
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Pathogenesis
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Bacteria from blood stream in any of the above mentioned routes are implanted on the cardiac valves or mural endocardium as they have surface adhesion molecules which mediate their adherence to endocardium
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Conditions predispose to implantation are –
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Previously damaged valves from diseases like RHD, congenital heart disease and prosthetic valves
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Hemodynamic stress
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These conditions causes damage to endothelium on valves, favoring the formation of platelet-fibrin thrombi which get infected from circulating bacteria where they proliferate and form vegetations
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Vegetations can embolize and as their embolic fragments contain virulent organisms, abscesses develop where they lodge, leading to sequelae such as septic infarcts or mycotic aneurysms
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Vegetations of subacute endocarditis are associated with less valvular destruction than acute endocarditis
Reference
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Vinay kumar, Abul K.Abbas, Nelson Fausto, Jon C. Aster. Robbins and Cotran Pathologic basis of disease. 8th edition