Clinical Description

IE is described as acute or subacute and is further delineated as left-sided, right-sided, native valve, or prosthetic valve. These distinctions help clinicians determine the most likely pathogen and chose appropriate empiric therapy. Right-sided IE occurs in only 5-10% of patients. IVDAs compromise the majority of these patients, and the prevalence of disease in these patients is 30 times that of the general population. Interestingly, 5-10% of patients are not addicts (2,3). Hospitalization appears to increase the risk of right-sided IE among non-IVDA patients. Risk factors in this setting include intravenous and intracardiac catheterization, abdominal surgery, hyperalimentation, and indwelling pacemakers (4-6).

Left-sided IE occurs more frequently than right-sided IE. Patients typically have underlying cardiac abnormalities (acquired or congenital), prosthetic valves, poor dentition, and/or HIV infection. Dental, respiratory, genitourinary, or gastrointestinal procedures may also predispose high-risk patients (those with underlying valvular abnormalities). Infection with highly virulent organisms such as staphylococci and Pseudomonas spp. can cause IE in the absence of underlying risk factors or cardiac abnormalities (2,3,7,8).

The clinical presentations of IE are variable and depend upon the pathogen, the duration of infection, the heart valves affected, and the mode of disease acquisition. Clinical manifestations include bacteremia and systemic embolization. Vasculitis is a more prominent feature of subacute bacterial endocarditis (SBE) because immune complexes do not have time to form in acute IE (1,9,10). Fever is the most frequent finding in patients with IE, and this diagnosis should be entertained in patients with fever of unknown origin. It is noteworthy, however, that roughly 19% of patients with culture-negative IE are afebrile (11). Associated nonspecific symptoms of IE include

From: Management of Antimicrobials in Infectious Diseases Edited by: A. G. Mainous III and C. Pomeroy © Humana Press Inc., Totowa, NJ

weight loss, chills, night sweats, malaise, fatigue, nausea, cough, and arthralgias. Elderly patients may have few symptoms, and their ability to mount a febrile response may be blunted (1,2,4,12,13). Other clinical manifestations may include neurologic symptoms (stroke or focal deficits due to embolic phenomenon), mental status changes, subarachnoid hemorrhage (secondary to mycotic aneurysm rupture), splenomegaly (abscess or infarct), and flank tenderness (renal infarcts)(1,2,12).

A variety of cardiac complications may evolve in IE, including myocarditis, perivalvular abscess formation, mycotic aneurysm formation, and conduction defects. In addition, myocardial infarction may occur as a result of coronary artery embolism (2,14). The presence of new or changing insufficiency murmurs may also develop; however, their absence does not exclude the diagnosis of IE. Right-sided murmurs are rare and their presence should further heighten the suspicion of IE (2,4,7,12,15). Another important cardiac complication is congestive heart failure, frequently out of proportion to or in the absence of valvular abnormalities. This may be secondary to microbial antigenic mimicry resulting in the formation of antibodies directed against myocardial proteins (16).

The vasculitis observed in SBE is a consequence of immune complex formation and deposition. This occurs predominately in the kidney, spleen, and skin (16). The clinical presentation may be dominated by isolated immunologic phenomena without other signs and symptoms (17). Renal involvement can result in glomerulonephritis with subsequent hematuria, proteinuria, and urinary red cell casts (1,4,12,16,18). Cutaneous lesions including petechiae and splinter hemorrhages develop in as many as half of patients; however, these findings are neither sensitive nor specific for SBE. Osler's nodes—small, tender nodules found on the pads of the fingertips—are uncommon but may appear later in the course of the disease (1,2,7,12,18). Janeway lesions are nontender macules that form on the fingers, palms, and soles. They are another uncommon cutaneous manifestation of IE that may result from systemic septic embolization or hypersensitivity angiitis (2).

Systemic embolization complicates the clinical picture in 22-50% of patients with IE (9). Patients with right-sided valvular vegetations may develop complications including pulmonary embolism, pneumonia, pulmonary hypertension, and lung abscess formation (1,2,4). In contrast, left-sided vegetations embolize to the major arterial beds in the central nervous system (CNS), heart, spleen, bowel, and extremities. This typically results in ischemia, infarction, hemorrhage, or abscess formation in the involved organ (1,2,5,7,9,12,19). Embolic events appear to be more common in left-sided IE and in IE caused by S. aureus, Candida spp., and the HACEK organisms (7,9,20).

Laboratory abnormalities frequently observed in patients with IE include an elevation in erythrocyte sedimentation rate, positive rheumatoid factor, cryoglobulinemia, leukocytosis, anemia, and elevations in blood urea nitrogen and creatinine (1,4,7,16,17). It is important to keep in mind that these abnormalities are not sensitive or specific in diagnosing IE, as they may also be present in a variety of other diseases.

The Duke criteria for the diagnosis of IE classify patients suspected of having IE into three categories based on the presence of specific pathologic and clinical criteria (9,19) (Table 1). Definite IE requires the culture or histological demonstration of microorganisms in a vegetation or intracardiac abscess or histological evidence of

Table 1

Duke's Clinical Criteria for Diagnosis of Infective Endocarditis

Major Criteria

Positive blood culture (no. 1 or 2)

1. Typical microorganisms consistent with IE from two separate blood cultures:

a. S. viridans, S. bovis, or HACEK group, or b. Community-acquired S. aureus or enterococci in absence of primary focus

2. Microorganisms consistent with IE from persistently positive blood cultures:

a. At least two positive cultures of blood samples drawn at least 12 h apart b. All of three or a majority of at least four separate blood cultures with first and last sample drawn at least 1 h apart

Evidence of endocardial involvement (no. 1 or 2)

1. Positive echocardiogram for IE defined as a. Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or b. Abscesses, or c. New partial dehiscence of prosthetic valve

2. New valvular regurgitation (worsening or changing of preexisting murmur not sufficient)

Minor Criteria

1. Predisposition: IVDA or predisposing heart condition

2. Fever: temperature of at least 38° Centigrade

3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions

4. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor

5. Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE

6. Echocardiographic findings: consistent with IE but do not meet a major criterion as noted above

Data from ref. 19.

endocarditis in a vegetation or intracardiac abscess. In addition, the patient must manifest two major criteria, one major and three minor criteria, or five minor criteria (Table 1). When criteria for definite IE are lacking but the diagnosis cannot be rejected, the patient is considered to have possible IE. The diagnosis is rejected when there is a resolution of clinical manifestations within 4 d of antibiotics, when there is no pathological evidence of disease after at least 4 d of antibiotics, and when there is a firm alternate diagnosis to explain the symptoms (19).

Bacteremia is a major diagnostic criterion of IE; however, 1-5% of patients will have negative blood cultures. Culture-negative IE occurs predominately in patients infected with members of the HACEK group and in those with IE due to unusual organisms such as Chlamydia or fungi, as these microorganisms may often take weeks to grow in culture with current techniques (1,7,9,11,21). Culture-negative IE may also result from the initiation of antimicrobial therapy prior to culturing the blood. In fact, administration of antibiotics prior to obtaining blood cultures may reduce bacterial recovery rate by 35-40% (1,9,22). Patients with culture-negative IE appear to have higher mortality rates, especially those with prosthetic valve endocarditis (PVE). This is presumably due to the delay in diagnosis and treatment (7,23).

Echocardiographic findings are also essential to the diagnosis of IE by the Duke criteria (19). Echocardiography has been particularly instrumental in the diagnosis of IE in patients with right-sided IE and culture-negative IE (7). Transthoracic echocardiog-raphy (TTE) has played an important diagnostic role in the initial management of patients suspected of having IE. It is rapid, noninvasive, and highly specific for detecting valvular vegetations (24). A major disadvantage of TTE is its low degree of sensitivity, and negative testing necessitates further imaging in patients strongly suspected of having IE. Furthermore, the ability of TTE to detect PVE and perivalvular abscess formation is limited. The usefulness of TTE is also limited in diagnosing IE in patients who have chronic obstructive pulmonary disease and in patients who are obese (2,9,24). Despite these shortcomings, a good quality TTE is still recommended as the initial procedure of choice for patients in whom the suspicion of IE is low (9).

Transesophageal echocardiography (TEE) has greater sensitivity than TTE, while maintaining a high degree of specificity, especially in patients with PVE (1,2,7,9,20,24). The most recent American Heart Association (AHA) guidelines recommend TEE as the procedure of choice in patients suspected of having PVE, for patients in whom the diagnosis of IE is intermediate or high, in patients who are difficult to image, and in patients with a high risk of complications (9).

Despite its high degree of sensitivity and specificity, TEE may be falsely negative in cases where vegetations are smaller than the limits of resolution, embolization of vegetations has occurred, or views are inadequate to detect small abscesses (10,24). Patients strongly suspected of having IE should undergo repeat TEE 7-10 d after an initially negative test (9). In patients who have undergone both TTE and TEE, the negative predictive value approximates 95% (10).

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