INFECTIVE ENDOCARDITIS/BACTERIAL ENDOCARDITIS
Infective endocarditis refers to the development of contaminated vegetations on the endocardium. The most common sites of involvement are the heart valves (including prosthetics) and the mural endocardium; however, aneurysmal sacs, the aorta, and other blood vessels may be affected. Male patients are affected more often than females, and the geriatric population (age greater than 65 years) are at a much higher risk. Valvular lesions are the most common and usually occur on damaged valves. The left side of the heart is more often affected than the right. When the cardiac endothelium is damaged, sterile platelet-fibrin thrombi develop and progress to form vegetations. During an episode of bacteremia, these vegetations become the site of colonization and growth of the infecting organism. Marantic endocarditis is a rarely encountered sterile form of disease and is seen most often in the chronically ill patient (usually associated with an underlying malignancy). Other forms of noninfective endocarditis are seen with systemic lupus erythematosus (Libman-Sacks endocarditis), Still’s disease, Reiter’s syndrome, and ankylosing spondylitis.
Patients with valvular abnormalities are at an increased risk for endocarditis. Both acquired (rheumatic disease, hypertrophic subaortic stenosis, mitral valve prolapse, sclerotic valve disease, and calcific valve disease) and congenital (ventricular septal defect, tetralogy of Fallot, coarctation of the aorta, patent ductus arteriosus) valvular lesions are associated with an increased incidence of endocarditis. Other high-risk patients include those with a prior history of endocarditis and surgically constructed systemic pulmonary shunts. Patients with any of these abnormalities are at risk of infection when undergoing invasive medical/ dental procedures or following trauma. Patients with prosthetic heart valves are also a high-risk population. Early prosthetic valve endocarditis occurs within 60 days of placement of the valve and is generally the result of intraoperative contamination. The most common etiologic agents are S. epidermidis and S aureus with gram negative aerobes, fungi (mostly Candida and Aspergillus species), streptococci, enterococci and diphtheroids responsible for a minority of cases. By contrast, late prosthetic valve endocarditis occurs after the valve has undergone endothelialization (greater than 60 days after implant) and results when transient bacteremia occurs (usually after a minor invasive procedure such as dental, genitourinary or gastrointestinal manipulation). Associated pathogens are similar to those seen with native valve endocarditis with Streptococci viridans being the most common. Dialysis patients are also at high risk for bacteremia and resultant endocarditis.
Acute bacterial endocarditis has an acute onset and manifests with more severe symptoms. Symptoms develop and progress over a one-week period and include chills, fever, myalgias and arthralgias. In contrast, subacute bacterial endocarditis has a more prolonged development with vague symptoms. The acute form of disease is encountered when the more virulent organisms are responsible for infection and it has a higher association of metastatic spread.
Bacteria are the most common infecting organisms; however, fungi, viruses, chlamydia, and rickettsia may also be responsible. Virtually any bacterial infection may result in endocarditis; however, streptococcus and staphylococcus species adhere more readily to cardiac valves than do gram-negative bacilli and therefore are the more commonly encountered etiologic agents. Two populations in which gram-negative bacilli and fungi are encountered more frequently are intravenous drug abusers and patients with prosthetic heart valves. Streptococcus viridans (accounts for the majority of cases) and Staphylococcus aureus cause most cases of native valve endocarditis. When the diagnosis seems certain but culture results are negative, consider unusual pathogens with slow growth or special growth requirements. The acronym HACEK (Haemophilus parainfluenzae, H. aphrophilus, H. paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominins, Eikenella corrodens, and Kingella kingae) refers to organisms which are encountered in culture negative endocarditis but are responsible for infection in approximately 5 to 10% of cases. Other unusual pathogens which may be inferred from the history include Coxiella burnetti (contact with sheep, cattle, and wild rabbits), Bartonella henselae (feline contact), and Chlamydia psittaci (contact with birds). As stated above, fungal elements should be suspected in cases of culture negative endocarditis in patients who inject drugs or who have prosthetic heart valves.
Laboratory abnormalities may include an elevated ESR, normocytic anemia, leukocytosis, bandemia, thrombocytopenia, false-positive nontreponemal syphilis serologies, positive rheumatoid factor assay, hematuria, or proteinuria. Blood cultures should be drawn as soon as the diagnosis is suspected. In subacute disease, three separate blood cultures should be drawn over a 24 hour period prior to initiating antibiotics. If urgent antibiotic therapy is deemed necessary, three separate cultures should be drawn over a one hour period and then therapy with intravenous antibiotics should be instituted.
The development of a new murmur often leads to the suspicion of endocarditis in most cases; however, in rare cases, a murmur may not be detected. Symptoms of congestive heart failure may develop as valvular damage worsens and progresses to either perforation of a leaflet, rupture of the chordae tendineae, or the development of stenosis from an obstructing vegetation. Other cardiac complications include valvular ring abscesses, myocardial infarction, myocarditis, and sudden death (seen more often in endocarditis secondary to intravenous drug abuse). Electrocardiography may show prolongation of the PR interval or complete heart block. Infectious emboli may result in metastatic spread to the lungs, brain, spleen, intestines, extremities, and eyes. The list of associated systemic symptoms is long, exhaustive and nonspecific (malaise, fatigue, night sweats, anorexia, weight loss, etc.). Some symptoms, which are more specific to endocarditis include Roth’s spots, digital clubbing, subungual splinter hemorrhages, petechiae, Janeway lesions, Osler’s nodes and splenomegaly. Echocardiography is used to establish the presence of cardiac vegetations in suspected cases. With transesophageal echocardiography the preferred method over transthoracic. Diagnostic criteria are used to establish the diagnosis based on major and minor diagnostic criteria.
Treatment is with prolonged courses of antibiotics. Appropriate antibiotic therapy should be guided by the results of sensitivity testing. However, these results are not available at presentation so therapy with either nafcillin (2 grams IV Q 4 hours) or penicillin G (2-3 million units IV Q 4 hours) along with gentamicin (1 mg/kg IV Q 8 hours) should be started empirically. In penicillin sensitive patients, vancomycin (15 mg/kg IV Q 12 hours) plus gentamicin (1 mg/kg IV Q 8 hours) is an acceptable alternative. Severe cases as manifest by rapidly progressive heart failure usually require surgical intervention. Other possible indications for surgery include persistent bacteremia despite antibiotic therapy, relapsing disease, multiple embolic phenomenon, heart block, rupture of the chordae tendoneae, papillary musculature, sinus of Valsalva or ventricular septum, cardiac abscess formation, or when associated with prosthetic valves which are recently placed, unstable or show signs of leakage. Recurrance is a great concern, and patients who have suffered endocarditis should be counseled to receive antibiotic prophylaxis prior to high-risk procedures.