Bacterial endocarditis refers to infection of the endocardial surface of the heart. It usually involves heart valves, but it can occur on the endocardium or intracardiac devices.
There are two types:
Most cases are caused by viridans streptococci, Streptococcus gallolyticus, Staphylococcus aureus, coagulase-negative staphylococci, HACEK organisms (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella), and enterococci. Rarer organisms include pneumococci, Candida, gram-negative bacilli, and polymicrobial organisms.
In developed countries, the incidence of endocarditis ranges from 2.6 to 7 cases per 100,000 population per year. The median age of patients with endocarditis is 58 years.
Age greater than 60 years, male gender, injection drug use, history of prior infective endocarditis, poor dentition or dental procedure, presence of a prosthetic valve or intracardiac device, history of valvular disease (rheumatic heart disease, mitral valve prolapse, aortic valve disease, mitral regurgitation, etc), congenital heart disease (aortic stenosis, bicuspid aortic valve, pulmonary stenosis, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, and tetralogy of Fallot), indwelling intravenous catheter, immunosuppression, hemodialysis patients.
Endothelial injury allows for either direct infection by virulent organisms or the development of uninfected platelet-fibrin thrombus which becomes a nidus for transient bacteremia, except in the case of S. aureus, which can infect intact endothelium. These organisms enter the bloodstream from the skin, mucosal surfaces or previously infected sites and adhere to nonbacterial thrombus due to valvular damage or turbulent blood flow. In the absence of host defenses, this organism is allowed to proliferate forming small colonies and shed in the bloodstream. Left-sided infection is much more common than right-sided infection, except among intravenous drug users.
Fever is the most common symptom. It can be associated with chills, night sweats, anorexia, weight loss, loss of appetite, malaise, headache, myalgias, arthralgias, abdominal pain, dyspnea, cough, and pleuritic pain.
Cardiac murmurs are observed in about 85% of patients. Congestive heart failure develops in 30% to 40% of patients usually due to valvular dysfunction. Other signs include cutaneous manifestations such as petechiae or splinter hemorrhages (non-blanching linear reddish-brown lesions under the nail bed).
Complications include conduction disease (first-degree atrioventricular block, bundle branch block, or complete heart block), ischemia (emboli to the coronary arteries), embolic stroke, intracerebral hemorrhage, brain abscess, septic emboli leading to infarction of the kidneys, spleen, lungs and other organs, hematogenous spread of infection leading to vertebral osteomyelitis, septic arthritis, or psoas abscess and systemic immune reaction such as glomerulonephritis.
Definite Infective Endocarditis
Pathologic criteria: Pathologic lesions such as vegetation or intracardiac abscess demonstrating active endocarditis on histology or microorganisms demonstrated by culture or histology of vegetation or intracardiac abscess
Clinical criteria: Two major clinical criteria or one major and three minor clinical criteria or five minor clinical criteria
Possible infective Endocarditis
One major and one minor clinical criteria or the presence of three minor clinical criteria
Rejected Diagnosis of Infective Endocarditis
If an alternate diagnosis is established, if there is the resolution of clinical manifestations with less than or equal to 4 days of antibiotic therapy, if there is no pathological evidence of infective endocarditis found at surgery or autopsy after antibiotic therapy for enterococci 4 days, or if clinical criteria for possible or definite infective endocarditis is not met
Major Clinical Criteria:
Positive blood cultures (one of the following):
Evidence of endocardial involvement (one of the following):
Minor Clinical Criteria:
At least three sets of blood cultures, separated from one another by at least 1 hour, should be obtained from separate venipuncture sites before initiation of antibiotic therapy. If cultures remain negative after 48 to 72 hours, two or three additional blood cultures should be obtained.
Culture-negative endocarditis is defined as endocarditis with no definitive microbiologic etiology after at least three independently obtained blood cultures. Up to 14% of patients may have negative blood cultures due to previous antibiotics therapy or due to fastidious organisms such as Coxiella, Legionella, Bartonella, Mycoplasma, Brucella, Chlamydia, and fungi.
Echocardiography should be performed in all patients with suspected bacterial endocarditis. In general, transthoracic echocardiography (TTE) is the first diagnostic test; however, transesophageal echocardiography (TEE) has higher sensitivity than TTE and is better for detection of cardiac complications such as abscess, leaflet perforation, and pseudoaneurysm. TTE is inadequate for detecting small vegetations (less than 2 mm), evaluating prosthetic valves and may be technically inadequate due to lung disease or body habitus.
Patients with a negative TEE for whom the clinical suspicion for IE is high should undergo repeat TEE 7 to 10 days later. Repeat TEE is also warranted after an initial positive TEE if clinical features suggest the new development of an intracardiac complication.
Laboratory data are usually nonspecific. Positive findings may include elevated inflammatory markers (erythrocyte sedimentation rate and/or elevated C-reactive protein), normochromic-normocytic anemia, positive rheumatoid factor, hypergammaglobulinemia, cryoglobulinemia, circulating immune complexes, hypocomplementemia, and false-positive serologic tests for syphilis. Urinalysis may demonstrate proteinuria, microscopic hematuria, and/or pyuria.
Empiric antibiotic therapy should cover Staphylococcus (methicillin-susceptible and resistant), Streptococcus, and Enterococcus. Initial treatment with vancomycin and gentamicin should cover a number of organisms prior to results of blood cultures.
The duration of therapy depends on the pathogen and site of valvular infection. The duration of therapy should be counted from the first day of negative blood cultures. Most patients are treated parenterally with regimens for up to 6 weeks.
Patients with relapse of native valve endocarditis following completion of appropriate antimicrobial therapy should receive a repeat course of antibiotics.
Treatment of specific organisms:
If nonsevere penicillin allergy: cefazolin
If severe penicillin allergy: vancomycin and daptomycin
Methicillin-resistant S. aureus or coagulase-negative staphylococci: vancomycin for 6 weeks
Viridans streptococci and S. gallolyticus: penicillin G or ceftriaxone for 4 weeks.
If penicillin-resistant: penicillin G for four weeks plus gentamicin for the first two weeks.
Penicillin allergy: vancomycin
S. pneumoniae: penicillin G, cefazolin, or ceftriaxone for four weeks
Penicillin allergy: vancomycin
Enterococcal species: penicillin or ampicillin plus gentamicin for 4 to 6 weeks
Penicillin allergy: vancomycin plus gentamicin for 6 weeks.
Vancomycin-resistant enterococcus: linezolid or quinupristin-dalfopristin or imipenem
HACEK organisms: ceftriaxone, ampicillin or ciprofloxacin for 4 weeks