Clinical Manifestations of Infective Endocarditis
المؤلف:
Longo, D., Fauci, A. S., Kasper, D. L., Hauser, S., Jameson, J. L., Loscalzo, J., Holland, S. M., & Langford, C. A.
المصدر:
Harrisons Principles of Internal Medicine (2025)
الجزء والصفحة:
22e , p1038-1039
2025-08-15
209
The highly variable clinical IE syndrome spans a continuum between acute and subacute presentations. Most forms of IE share clinical and laboratory manifestations (Table 1). The causative microorganism is primarily responsible for the temporal course of IE. β-Hemolytic streptococci, S. aureus, and pneumococci typically result in an acute course, and IE caused by Staphylococcus lugdunensis (a coagulase negative species) or by enterococci may present acutely. Subacute IE is typically caused by viridans streptococci, enterococci, CoNS, and the HACEK group. IE caused by Bartonella species, T. whipplei, C. burnetii, or M. chimaera is exceptionally indolent.
Table1. Clinical and Laboratory Features of Infective Endocarditis
In patients with subacute presentations, fever is typically low-grade, rarely exceeding 39.4°C (103°F); in contrast, temperatures of 39.4° 40°C (103°–104°F) are often noted in acute IE. Fever may be blunted in patients who are elderly, are severely debilitated, or have renal failure.
Cardiac Manifestations Although heart murmurs are usually indicative of the predisposing cardiac pathology rather than of IE, valvular damage and ruptured chordae may result in new regurgitant murmurs. In acute IE involving a normal valve, murmurs may be absent initially but ultimately are detected in 85% of cases. Congestive heart failure (CHF) resulting from valve dysfunction or, occasionally, intracardiac fistulae develop in 30–40% of patients. Extension of leaflet infection into adjacent annular or myocardial tissue results in paravalvular abscesses, which in turn may cause intracardiac fistulae with new murmurs. Aortic paravalvular infection may burrow into the upper ventricular septum and interrupt the conduction system, leading to varying degrees of heart block. Mitral paravalvular abscesses are more distant from the conduction system and rarely cause conduction abnormalities. Coronary artery emboli occur in 2% of patients and may result in myocardial infarction.
Noncardiac Manifestations The classic nonsuppurative peripheral manifestations of subacute IE (e.g., Janeway lesions; Fig. 1A) are related to prolonged infection; with early diagnosis and treatment, these have become infrequent. In contrast, septic embolization mimicking some of these lesions (subungual hemorrhage, Osler’s nodes) is common in patients with acute S. aureus IE (Fig. 1B). Musculoskeletal pain usually remits promptly with treatment but must be distinguished from focal metastatic infections (e.g., spondylodiscitis), which may complicate 10–15% of cases. Hematogenously seeded focal infection occurs most often in the skin, spleen, kidneys, skeletal system, and meninges. Arterial emboli, one-half of which precede the diagnosis of IE, are clinically apparent in up to 50% of patients. S. aureus IE, mobile vegetations >10 mm in diameter, and infection involving the mitral valve anterior leaflet are independently associated with an increased risk of embolization. Embolic arterial occlusion causes regional pain or ischemia-induced organ dysfunction (e.g., of the kidney, spleen, bowel, extremity). Cerebrovascular emboli presenting as strokes or occasionally as encephalopathy complicate 15–35% of cases; however, evidence of clinically asymptomatic emboli is found on magnetic resonance imaging (MRI) in 30–65% of patients with left-sided IE. The frequency of stroke is 8 per 1000 patient-days during the week prior to diagnosis and decreases to 4.8 and 1.7 per 1000 patient-days during the first and second weeks of effective antimicrobial therapy, respectively. Only 3% of strokes occur after 1 week of effective therapy. Emboli occurring late during or after effective therapy do not in themselves constitute evidence of failed antimicrobial treatment.
Fig1. A. Janeway lesions on the toe (left) and plantar surface (right) of the foot in subacute Neisseria mucosa infective endocarditis (IE). (Images courtesy of Rachel Baden, MD.) B. Septic emboli with hemorrhage and infarction due to acute Staphylococcus aureus IE.
Other neurologic complications include aseptic or purulent meningitis, intracranial hemorrhage due to hemorrhagic infarcts or ruptured mycotic aneurysms, and seizures. Mycotic aneurysms are focal dilations of arteries occurring at points in the artery wall that have been weakened by infection in the vasa vasorum or where septic emboli have lodged. Microabscesses in the brain and meninges occur commonly in S. aureus IE; intracerebral abscesses requiring surgical drainage are infrequent.
Immune complex deposition on the glomerular basement membrane causes diffuse hypocomplementemic glomerulonephritis and renal dysfunction, which typically improve with effective antimicrobial therapy. Embolic renal infarcts cause flank pain and hematuria but rarely renal dysfunction. Splenic infarcts or abscess can manifest as left upper abdominal, pleuritic chest, or left shoulder pain.
Manifestations with Specific Predisposing Conditions Among PWID, 35–60% of IE is limited to the tricuspid valve and presents with fever with faint or no murmur and without peripheral manifestations. Septic pulmonary emboli, which are common with tricuspid IE, cause cough, pleuritic chest pain, nodular pulmonary infiltrates, and occasionally empyema or pyopneumothorax. Infection of the aortic or mitral valve presents with the typical clinical features of IE, including peripheral manifestations.
Health care–associated IE has typical manifestations unless associated with an intracardiac device or masked by the symptoms of concur rent illness. CIED-IE may be associated with obvious (especially within 6 months of device manipulation) or cryptic generator pocket infection or arise through bacteremic seeding without pocket infection. Fever, sepsis, minimal murmur, and occasionally pulmonary symptoms due to septic emboli are seen. Late-onset PVE and TAVR-PVE present with typical clinical features. In early PVE, symptoms may be masked by recent surgery. In both early and late PVE, paravalvular infection is common and often results in partial valve dehiscence, regurgitant murmurs, CHF, or disruption of the conduction system.
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