The causative organisms differ depending on the underlying risk factors; 50% to 60% of cases occurring on damaged or deformed valves are caused by Streptococcus viridans, a relatively banal group of normal oral flora. By contrast, the more virulent S. aureus (common to skin) can attack healthy as well as deformed valves and is responsible for 10% to 20% of cases overall; it also is the major offender in infections occurring in intravenous drug abusers. Additional bacterial agents include enterococci and the so-called “HACEK group” (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella), all commensal in the oral cavity. More rarely, gram-negative bacilli and fungi are involved. In about 10% of all cases of endocarditis, no organism is isolated from the blood (“culture-negative” endocarditis) because of previous antibiotic therapy, difficulty in isolating the offending agent, or because deeply embedded organisms within the enlarging vegetation are not readily released into the blood.
Foremost among the factors predisposing to endocarditis is seeding of the blood with microbes. The mechanism or portal of entry of the agent into the bloodstream may be an obvious infection elsewhere, a dental or surgical procedure that causes a transient bacteremia, injection of contaminated material directly into the bloodstream by intravenous drug abusers, an occult source from the gut, or oral cavity, or trivial injuries. Recognition of predisposing anatomic substrates and clinical conditions causing bacteremia allows appropriate antibiotic prophylaxis.
MORPHOLOGYInbothacuteandsubacuteformsofthedisease,friable,bulky,andpotentiallydestructivevegetationscontainingfibrin,inflammatorycells,andmicroorganismsarepresentontheheartvalves(
Figs.11.20 11.21 ).The aortic and mitral valves are the most common sites of infection, although the tricuspid valve is a frequent target in the setting of intravenous drug abuse. Vegetationsmaybesingleormultipleandmayinvolvemorethanonevalve;theycansometimeserodeintotheunderlyingmyocardiumtoproduceanabscesscavity(ring abscess) (
Fig.11.21B ).Sheddingofemboli iscommonbecauseofthefriablenatureofthevegetations.Sincethefragmentedvegetationscontainlargenumbersoforganisms,abscessesoftendevelopatthesiteswhereembolilodge,leadingtodevelopmentofseptic infarcts andaneurysmsresultingfrombacterialinfectionofthearterialwall(mycotic aneurysms).
Subacuteendocarditistypicallycauseslessvalvulardestructionthanacuteendocarditis.Onmicroscopicexamination,thevegetationsofsubacuteendocarditisoftenhavegranulationtissueattheirbases(suggestingchronicity),promotingdevelopmentofchronicinflammatoryinfiltrates,fibrosis,andcalcificationovertime.
Fever is the most consistent sign of infective endocarditis.
However, in subacute disease (particularly in older adults), fever may be absent, and the only manifestations may be nonspecific fatigue, weight loss, and a flulike syndrome; splenomegaly also is common in subacute cases. By contrast, acute endocarditis often manifests with rapidly developing fever, chills, weakness, and lassitude. Murmurs are present in 90% of patients with left-sided lesions. In those who are not treated promptly, microemboli are formed, which can give rise to petechia, nail bed (splinter) hemorrhages, retinal hemorrhages (Roth spots), painless palm or sole erythematous lesions (Janeway lesions), or painful fingertip nodules (Osler nodes); diagnosis is confirmed by positive blood cultures and echocardiographic findings.