Infective Endocarditis Classification

• Infective endocarditis (IE) is an infection of the endocardium, most commonly affecting heart valves and adjacent structures.
• IE is caused by a wide variety of bacteria and fungi.
• Common sites for IE include heart valves, septal defects, chordae tendinae, and mural endocardium.
• IE is classified into acute and subacute forms.
• Acute bacterial endocarditis is caused by virulent organisms and runs its course over days to weeks.
• Subacute bacterial endocarditis is caused by organisms of low virulence and runs its course over weeks to months.
• IE involves the formation of vegetations, composed of platelets, fibrin, microorganisms, and inflammatory cells.
• The susceptible host for IE can occur at any age but is most common in older adults, with a median age of onset of 50 years and a male-to-female ratio of 2:1.
• Most patients have a preexisting cardiac condition that affects the valves.
• IV drug abusers have a high risk for IE, particularly for tricuspid valve infection caused by Staphylococcus aureus.
• The incidence of IE in a general population is between 2 and 6 cases per 100,000 persons-years, but it is higher in patients with underlying valvular heart diseases and those with IVDA.
• Mitral valve prolapse, aortic sclerosis, and bicuspid aortic valvular heart disease are now more frequent causes of IE than rheumatic valvulitis.
• Prosthetic valvular heart disease accounts for about one third of all cases of endocarditis.
• Staphylococcus aureus causes early cases of pacemaker endocarditis, while Staphylococcus epidermidis causes late cases.
• Infected surgical wounds and vascular catheter-associated bacteremias are significant risk factors for IE.
• Signs and symptoms of IE include fever and chills, dyspnea, cough, pleuritic chest pain, arthralgias, myalgias, new or changed heart murmurs, heart failure, and arrhythmias.
• Extracardiac manifestations of IE include peripheral embolic and immunologic phenomena, renal injury, splenomegaly, neurological manifestations, and arthritis.
• High clinical suspicion of IE includes new valve lesions or regurgitant murmurs, embolic events of unknown origin, sepsis of unknown origin, fever together with other risk factors, and haematuria or glomerulonephritis.
• The diagnosis of IE is based on a clinical suspicion supported by consistent microbiological data and the documentation of IE-related cardiac lesions by imaging techniques, such as echocardiography.
• Positive blood cultures remain the cornerstone of IE diagnosis and provide live bacteria for identification and susceptibility testing.
• Successful treatment of IE relies on microbial eradication by antimicrobial drugs and the removal of infected material by surgery.
• Bactericidal regimens are more effective than bacteriostatic therapy, and duration of treatment depends on the location of the infection.
• Empiric antibiotic therapy provides broad-spectrum coverage for potential bacterial causes of IE until blood culture results are available.
• Staphylococcus aureus is responsible for acute and destructive IE, while CoNS causes more protracted valve infections.
• Enterococcal IE is primarily caused by E. faecalis and Enterococcus faecium and requires prolonged administration of antimicrobial therapy.
• HACEK Gram-negative bacilli are fastidious organisms that require special investigations and are susceptible to ceftriaxone, other third-generation cephalosporins, and fluoroquinolones.
• Fungal IE is most frequently observed in PVE and in IE affecting PWID or immunocompromised patients, with high mortality and a need for combined antifungal administration and a low threshold for surgery.
• Persistent fever during the treatment of endocarditis is a cause for concern.

Test your knowledge on the classification of infective endocarditis, which is caused by a wide variety of bacteria and fungi and usually involves the heart valves and adjacent structures. Learn about acute bacterial endocarditis and subacute bacterial endocarditis.