Key Clinical Updates in Infective Endocarditis
Although intravenous therapy has been the mainstay of treatment for infective endocarditis, some data have begun to support the use of oral antibiotic therapy following 2 weeks of intravenous antibiotic regimens for certain organisms.
ESSENTIALS OF DIAGNOSIS
Preexisting organic heart lesion.
Positive blood cultures.
Evidence of vegetation on echocardiography.
Evidence of systemic emboli.
Endocarditis is a bacterial or fungal infection of the valvular or endocardial surface of the heart. The clinical presentation depends on the infecting organism and the valve or valves that are infected. More virulent organisms—S aureus in particular—tend to produce a more rapidly progressive and destructive infection. Endocarditis caused by more virulent organisms often presents as an acute febrile illness and is complicated by early embolization, acute valvular regurgitation, and myocardial abscess formation. Viridans strains of streptococci, enterococci, other bacteria, yeasts, and fungi tend to cause a more subacute picture (eFigure 33–8).
Large vegetations of the mitral valve leaflets from subacute bacterial endocarditis. (Public Health Image Library, CDC).
Underlying valvular disease, less common than in the past, is present in about 50% of cases. Valvular disease alters blood flow and produces jet effects that disrupt the endothelial surface, providing a nidus for attachment and infection of microorganisms that enter the bloodstream. Predisposing valvular abnormalities include rheumatic involvement of any valve, bicuspid aortic valves, calcific or sclerotic aortic valves, hypertrophic subaortic stenosis, mitral valve prolapse, and a variety of congenital disorders such as ventricular septal defect, tetralogy of Fallot, coarctation of the aorta, or patent ductus arteriosus. Rheumatic disease is no longer the major predisposing factor in developed countries. Regurgitation lesions are more susceptible than stenotic ones.
The initiating event in native valve endocarditis is colonization of the valve by bacteria or yeast that gain access to the bloodstream. Transient bacteremia is common during dental, upper respiratory, urologic, and lower gastrointestinal diagnostic and surgical procedures. It is less common during upper gastrointestinal and gynecologic procedures. Intravascular devices are also a portal of access of microorganisms into the bloodstream. A large proportion of cases of S aureus endocarditis are attributable to health care–associated bacteremia.
Native valve endocarditis is usually caused by S aureus, viridans streptococci, enterococci, or HACEK organisms (an acronym for Haemophilus aphrophilus [now Aggregatibacter aphrophilus], Actinobacillus actinomycetemcomitans [now Aggregatibacter actinomycetemcomitans], Cardiobacterium hominis, Eikenella corrodens, and Kingella species). Streptococcal species formerly accounted for the majority of native valve endocarditis cases; S aureus is now the leading cause. Gram-negative organisms and fungi account for a small percentage.
In injection drug users, S aureus accounts for over 60% of all endocarditis cases and for 80–90% of cases in which the tricuspid valve is infected. Enterococci and streptococci comprise the balance in about ...