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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjE2NjUwLXdvcmt1cA==\nDrugs & Diseases > Infectious Diseases\nInfective Endocarditis Workup\nAuthor: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD more...\nSections Infective Endocarditis\nBlood and Urine Studies\nBlood Culture\nAntibiotic Therapy\nManagement of S aureus Bacteremia\nAnticoagulation Therapy\nPrevention of Infective Endocarditis\nThe criterion standard test for diagnosing infective endocarditis (IE) is the documentation of a continuous bacteremia (>30 min in duration) based on blood culture results.\nAlthough blood cultures remain key in making the diagnosis of IE, the need for indirect diagnostic techniques that are both specific and sensitive is increasing. This is because the nature of valvular infections has changed over the years. The numbers of fastidious organisms have increased, and the rate of the classic peripheral stigmata of IE is much lower. Patients who are elderly, chronically ill, or immunosuppressed are often afebrile and unable to mount a significant fever or exhibit the classic stigmata of valvular infection.\nA major clinical challenge is that at least 25% of S aureus bloodstream infections (BSIs) represent IE or metastatic infections. The question is whether a continuous bacteremia in the presence of an intravascular line is representative of IE. Blood cultures should only be drawn through intravascular lines for the purpose of diagnosing catheter-related BSIs and have limited value for answering this clinical challenge.\nBecause of the ability of S aureus to produce an endotheliosis, the presence of a continuous bacteremia does not necessarily imply an infected valvular vegetation.\nAn important clue to continuous bacteremia/IE is the presence of S aureus bacteriuria associated with hematuria. Hematuria in the setting of IE is due to embolic renal infarction or immunologically mediated glomerulonephritis. Echocardiography has developed into a useful tool for meeting this clinical challenge.\nTwenty-five percent of patients with staphylococcal bacteremia and 23% of those with catheters as the primary focus have evidence of IE based on transesophageal echocardiography (TEE) findings, in the absence of clinical and transthoracic echocardiography (TTE) findings. [2]\nSend baseline studies, such as complete blood count (CBC), electrolytes, creatinine, blood urea nitrogen (BUN), glucose, and coagulation panel, to the laboratory for testing.\nAnemia is common in subacute endocarditis. Leukocytosis is observed in acute endocarditis. Erythrocyte sedimentation rate (ESR), while not specific, is elevated in more than 90% of cases. Decreased C3, C4, and CH50 are evident in subacute endocarditis.\nRheumatoid factor (ie, “poor man’s circulating immune complex”) becomes positive in 50% of patients with subacute disease. It becomes negative after successful treatment.\nProteinuria and microscopic hematuria are present in approximately 50% of cases.\nThe criterion standard test for diagnosing IE is the documentation of a continuous bacteremia (>30 min in duration) based on blood culture results.\nExceptions are observed in patients with prosthetic valve endocarditis (PVE) and right-sided IE. About 5-10% of patients with IE have false-negative blood culture results. Prior use of antibiotics is the most common cause of false-negative blood culture results. Other causes include fastidious organisms and inadequate blood volume; a blood-to-broth ratio of 1:10 is needed. Currently, with modern automated blood culture systems, fastidious organisms such as nutritionally variant streptococci and members of the HACEK group rarely cause culture-negative IE.\nAs many as 50% of positive blood culture results have been estimated to be falsely positive. This rate has probably decreased, but false-positive blood culture results remain a major diagnostic challenge. One such result can lead to 4 days of unnecessary patient hospitalization.\nThe significance of positive blood culture results correlates with the following:\nThe type of organism\nThe clinical setting (coagulase-negative staphylococci [CoNS] are significant in patients with prosthetic valves but not in those with native valves)\nMultiple blood cultures positive for the same organism\nShorter incubation time for recovery\nThe degree of severity of clinical illness\nNever draw only 1 set of blood cultures; 1 is worse than none. Two sets of blood cultures have greater than 90% sensitivity when bacteremia is present. Three sets of cultures improve sensitivity and may be useful when antibiotics have been administered previously.\nThe AHA (endorsed by IDSA) 2010 guideline update on CIED infections and their management recommends drawing at least 2 sets of blood cultures at evaluation before starting antimicrobial therapy. [43]\nFor diagnosing subacute IE, draw 3-5 sets of blood cultures over 24 hours. This helps detect 92-98% of cases in patients who have not recently received antibiotics. In the case of acute IE, 3 sets may be drawn over 30 minutes (with separate venipunctures) to help document a continuous bacteremia.\nUsing various types of blood culture bottles (with resins added to interfere with antibiotic action) probably has little advantage. Some of these may interfere with bacterial growth.\nWhen blood culture results fail to show an infectious agent after blood is drawn 48 hours after antibiotic therapy has been stopped, the second set of blood for cultures must be drawn approximately 7 days later. If these later culture results remain negative, the diagnosis of IE must be reconsidered. In general, blood for culture should not be drawn through intravenous (IV) lines unless this is part of an approach for diagnosing line infection.\nCatheter infection\nThe diagnosis of catheter infection may be made in 1 of 2 ways. Culturing the device via the roll-plate semiquantitative method is the most common approach but requires a catheter removal. In the case of long-term catheters, blood may be drawn simultaneously through the line and the peripheral vein. If it is impossible to draw blood from a peripheral vein in the presence of a multilumen catheter, one sample may be obtained through each of 2 catheter lumens.\nIn a catheter infection, the colony count of the sample obtained from the suspected port is 3-fold greater than that drawn from a peripheral vein or from another port of the catheter. Retrieval of organisms from blood drawn from a catheter hub at least 2 hours earlier before their growth is detected in the blood obtained from peripheral vein meets the differential time to positivity criteria of a catheter infection.\nA sterile culture of the insertion site has a highly negative predictive value for line infection.\nCulture-negative infective endocarditis\nApproximately 5% of cases of possible IE yield negative blood culture results (ie, culture-negative IE). Patients with culture-negative IE occasionally present with signs and symptoms highly suggestive of IE, but the blood cultures remain negative.\nCulture-negative IE may have noninfectious causes (eg, vasculitis) or may be caused by fastidious organisms. Modern blood culture systems recover the vast majority of pathogens within 4-5 days, including members of the HACEK group and Abiotrophia species. Overall, the most common cause of culture-negative IE is prior antimicrobial therapy that can suppress bacterial growth within the vegetation but is insufficient to eliminate the valvular infection.\nIn certain populations, infections with Coxiella burnetii (in southern France and Israel) and Bartonella species (among homeless persons) have become more frequent causes of culture-negative IE. The blood culture results in fungal valvular infections are often sterile. In S aureus IE, the blood cultures results may be negative when the organism burrows deep within the thrombus, leaving the surface of the valvular thrombus sterile (surface sterilization). [63]\nValvular vegetations may be detected during cardiac ultrasonographic examinations, but the blood culture results are persistently negative. In this situation, 3 separate blood cultures spaced over a 24-hour period are usually sufficient to detect microorganisms in the blood. Additional blood cultures are not usually helpful.\nMany pathogens once considered to be fastidious are no longer classified as such (see above). Bartonella, Legionella, and C burnetii remain significant causes of culture-negative IE. These require special culture media or a prolonged incubation period for retrieval.\nSerology for Chlamydia, Q fever (C burnetii), and Bartonella may be useful in culture-negative endocarditis. Serologic tests are often the most practical means for diagnosing valvular infection with fastidious organisms (eg, C burnetii and Chlamydia, Brucella, and Legionella species). Buffered charcoal and yeast agar are required for the isolation of Legionella. Brucella species require up to 6 weeks.\nIt appears that Tropheryma whippelii, which causes Whipple disease, is becoming a more common cause of culture-negative endocarditis. [64]\nThuny et al have developed an algorithm for the workup of negative blood cultures. The first stage is to obtain serologies for Q fever and Bartonella. Rheumatoid factor and antinuclear antibody testing is performed to rule out rheumatologic diseases. If testing is negative, then a dedicated PCR for Bartonella species and T whipplei should be performed as well as a broad range PCR for the detection of fungi, especially in the setting of a prosthetic valve. If there is no yield from this second tier, especially with a history of antecedent antibiotic therapy, then a Septifast blood PCR should be performed to detect any staphylococci. In addition, serologic testing for Mycoplasma pneumoniae, Legionella pneumophila and Brucella melitensis should be carried out. [65]\nFungal infective endocarditis\nMost types of fungal IE have a low rate of positive blood culture results. At best, only 50% of Candida species are associated with positive blood culture results. Histoplasma and Aspergillus are almost never retrieved from the bloodstream. Fungal endocarditis must always be considered in the clinical setting of culture-negative IE that fails to respond to appropriate antibiotic therapy.\nPacemaker infective endocarditis\nEstablishing the diagnosis of pacemaker IE is difficult because of its subtle presentation, especially late-onset disease. The addition of pocket infection and the presence of pulmonary emboli to the Duke criteria have increased the rate of diagnosis from 16% to 87.5% of cases. Fever and/or a positive blood culture result without evidence of a primary source in patients with a pacemaker or implantable cardioverter-defibrillator should be considered to represent device-associated IE until proven otherwise. [66, 67, 68, 69, 70, 71, 72]\nThe AHA 2010 guideline update on CIED infections recommends that, when the CIED is explanted, culture of the lead-tip and Gram stain and culture of the generator-pocket tissue be obtained. However, percutaneous aspiration of the generator pocket should not be performed for diagnostic evaluation of CIED infection. [43]\nEchocardiography has become the indirect diagnostic method of choice, especially in patients who present with a clinical picture of IE but who have nondiagnostic blood culture results (eg, some patients with fungal endocarditis). The diagnosis of IE can never be excluded based on negative echocardiogram findings, either from TTE or from TEE.\nThe AHA 2010 guideline update on CIED infections recommends TEE to evaluate the left-sided heart valves for all adults suspected of having CIED-related endocarditis, even if TTE has shown lead-adherent masses. If TTE views are good, TTE may be sufficient for pediatric patients. Patients with positive blood culture results or negative blood culture results taken after recent antimicrobial therapy should undergo TEE for CIED infection or valvular endocarditis. [43]\nVisible vegetation suggests a worse prognosis. Both TTE and TEE are highly specific for valvular vegetations; however, sensitivity differs.\nTwo-dimensional cardiac Doppler ultrasound testing has been a significant advance for the diagnosis and evaluation of IE. It provides information about the presence and size of vegetations, which helps in diagnosis and, to some extent, in predicting embolization.\nTTE is more sensitive for detecting anterior myocardial abscesses and quantitating the degree of valvular dysfunction.\nThe Doppler method can be used to detect distorted blood flow and certain types of cardiac pathology not otherwise visualized by standard echocardiography. It is good for visualizing jet lesions and differentiating cusp perforation from valvular insufficiency.\nThe combination of TEE and color Doppler is excellent for detecting intracardiac fistulas. The resolution of both TEE and TTE in real time is approximately 2 mm.\nConditions that are positively related to the detection of valvular thrombi include the location (ie, right-sided structures are poorly visualized, especially by TTE); disease lasting longer than 2 weeks; abscesses of the valves or myocardium; and aneurysms of the sinus of Valsalva.\nTTE (see the image below) has generally had a sensitivity of approximately 60% for identification of valvular lesions in patients with native valve endocarditis (NVE). However, sensitivity was as high as 82% in a recent series where advanced harmonic imaging and digital processing techniques were used. [73] TTE has a sensitivity of only 20% in patients with PVE.\nThis is a magnified portion of a parasternal long axis view from a transthoracic echocardiogram. There is a small curvilinear vegetation on the mitral valve as indicated. The patient presented with a headache and fever, and CT scan of the brain revealed an occipital hemorrhage. The patient had a history of intravenous drug use and multiple blood cultures grew Staphylococcus aureus.\nTEE was developed to overcome the problems in visualizing prosthetic valve thrombi and right-sided events. TEE eliminates the need for the operator to find a clear field for the beam. The use of higher-frequency waveforms is permitted because of the decreased distance between the heart and the probe. The sensitivity of TEE in detecting the vegetations of NVE is 90-100%. In patients with PVE, the sensitivity of TEE under optimal circumstances is greater than 90%.\nTEE successfully visualizes vegetations of the leads or of the tricuspid valve in more than 90% of cases of pacemaker IE, compared with less than the 50% achieved by TTE.\nNeither TEE nor TTE should be used for screening purposes (ie, patients with fever of unknown origin or those with positive blood culture results and no other signs or symptoms of IE), because nearly 60% of vegetations revealed are sterile. Approximately 15% of positive study results are false-positives because the images are, in reality, not those of vegetations but of thickened valves, nodules, or valvular calcifications.\nEchocardiography is useful for predicting the potential complications of IE, especially those that are embolic in nature.\nEchocardiographic predictors of systemic embolization in patients with IE are the following:\nLarge valvular vegetations (>10 mm in diameter)\nMultiple vegetations\nMobile but pedunculated vegetations\nNoncalcified vegetations\nVegetations that are increasing in size\nProlapsing vegetations\nEchocardiography is also highly useful for detecting abscesses. As with valvular lesions, the transesophageal technique is generally more sensitive. [74]\nIn summary, the indications for performing echocardiography with Doppler in patients with IE are to provide a baseline in proven or highly suggestive cases of IE and to provide a means of documenting complications during therapy.\nIn most cases, TTE is sufficient. TEE is indicated when mechanical prosthetic valves are present; to detect right-sided lesions; and to visualize myocardial abscesses. Because of the endoscopic portion of the test, TEE carries the risk factor of inducing bacteremias. Approximately 15% of cases of IE do not demonstrate any detectable vegetations at the time of the echocardiographic study.\nTwo-dimensional cardiac Doppler ultrasound testing has been a significant advance for diagnosing and evaluating IE. It provides information about the presence and size of vegetations, which helps in diagnosis and, to some extent, in predicting embolization.\nTTEs are more sensitive for detecting anterior myocardial abscesses and quantitating the degree of valvular dysfunction.\nThe Doppler method can detect distorted blood flow and certain types of cardiac pathology not otherwise visualized by standard echocardiography. It is good for visualizing jet lesions and differentiating cusp perforation from valvular insufficiency.\nThe combination of TEE and color Doppler is excellent for detecting intracardiac fistulas. The resolution of either TEE or TTE in real life is approximately 2 mm.\nConditions that are positively related to the detection of valvular thrombi are the location (ie, right-sided structures are poorly visualized, especially by TTE); disease lasting longer than 2 weeks; abscesses of the valves or myocardium; and aneurysms of the sinus of Valsalva.\nPulmonary embolic phenomena on radiographs strongly suggest tricuspid disease (see the image below).\nA young adult with a history of intravenous drug use, endocarditis involving the tricuspid valve with Staphylococcus aureus, and multiple septic pulmonary emboli. Pulmonary lesions on chest radiograph are most prominent in the right upper lobe with both solid and cavitary appearance.\nMultiple embolic pyogenic abscesses may be visualized.\nVentilation/perfusion scanning may be useful in right-sided endocarditis.\nElectrocardiography may help detect the 10% of patients who develop a conduction delay during IE by documenting an increased P-R interval. Nonspecific changes are common. First-degree atrioventricular (AV) block and new interventricular conduction delays may signal septal involvement in aortic valve disease; both are poor prognostic signs.\nCatheterization of the heart is rarely required for the diagnosis of IE or any of its complications, though it may be indicated to determine the degree of valvular damage. The findings from echocardiography correlate well with the findings from cardiac catheterization. The characteristic findings of IE are intravascular endocardial vegetations that contain microorganisms surrounded by fibrin and platelets.\nVarious radionuclide scans using, for example, gallium (Ga)-67–tagged white cells and indium (In)-111–tagged white cells, have proven to be of little use in diagnosing IE. Radionuclide scans of the spleen are useful to help rule out a splenic abscess, which is a cause of bacteremia that is refractory to antibiotic therapy.\nA computed tomography (CT) scan of the head should be obtained in patients who exhibit central nervous system (CNS) symptoms or findings consistent with a mass effect (eg, macroabscess of the brain). [75, 76, 77] This imaging modality has proven most useful for localizing abscesses. With new advanced multislice techniques, CT can now also be used to identify valvular abnormalities and vegetations. [78]\nAn increasing amount of evidence supports the advantages of fluorine-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) scanning over electrocardiographically gated computed tomographic angiography (CTA) in certain circumstances. PET scanning may facilitate earlier diagnoses of infected intracardiac devices and prosthetic valves than do these other studies. [79]\nEpaulard O, Roch N, Potton L, Pavese P, Brion JP, Stahl JP. Infective endocarditis-related stroke: diagnostic delay and prognostic factors. Scand J Infect Dis. 2009. 41(8):558-62. [Medline].\nDurack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. 1994 Mar. 96(3):200-9. [Medline].\nBrusch JL. Infective endocarditis and its mimics in the critical care unit. Cunha BA, ed. Infectious Diseases in Critical Care. 2nd ed. New York, NY: Informa Healthcare; 2007. 261-2.\nKarchmer AW. 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Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation. 2005 Jun 14. 111(23):e394-434. [Medline].\nBuckholz K, Larsen CT. Severity of gentamicin is nephrotoxic effect on patients with infective endocarditis: a prospective observation of cohort study of 373 patients. Clinical Infect Dis. 2009. 48:65-71.\nCunha BA. Persistent S. aureus acute bacteremia: clinical pathway for diagnosis and treatment. Antibiot for Clin. 2006. 10:39-46.\nFalagas ME, Manta KG, Ntziora F, Vardakas KZ. Linezolid for the treatment of patients with endocarditis: a systematic review of the published evidence. 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Telephone consultation cannot replace bedside infectious disease consultation in the management of Staphylococcus aureus Bacteremia. Clin Infect Dis. 2013 Feb. 56 (4):527-35. [Medline].\nNishimura RA, Carabello BA, Faxon DP, Freed MD, Lytle BW, O’Gara PT, et al. ACC/AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. Aug 2008. 118(8):887-96.\nNetzer RO, Altwegg SC, Zollinger E, Täuber M, Carrel T, Seiler C. Infective endocarditis: determinants of long term outcome. Heart. 2002 Jul. 88(1):61-6. [Medline]. [Full Text].\n[Guideline] Baddour LM, Wilson WR, Bayer AS, et al. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. 2015 Oct 13. 132 (15):1435-86. [Medline].\nUS Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when linezolid (Zyvox®) is given to patients taking certain psychiatric medications. Available at http://www.fda.gov/Drugs/DrugSafety/ucm265305.htm. Accessed: July 27, 2011.\nBoggs W. Ampicillin-Ceftriaxone Effective for E. faecalis Endocarditis. Medscape. Feb 12 2013. Available at http://www.medscape.com/viewarticle/779187.\nFernández-Hidalgo N, Almirante B, Gavaldà J, Gurgui M, Peña C, de Alarcón A, et al. Ampicillin Plus Ceftriaxone Is as Effective as Ampicillin Plus Gentamicin for Treating Enterococcus faecalis Infective Endocarditis. Clin Infect Dis. 2013 Feb 25. [Medline].\nYong MS, Saxena P, Killu AM, Coffey S, Burkhart HM, Wan SH, et al. The Preoperative Evaluation of Infective Endocarditis via 3-Dimensional Transesophageal Echocardiography. Tex Heart Inst J. 2015 Aug. 42 (4):372-6. [Medline].\nAcute bacterial endocarditis caused by Staphylococcus aureus with perforation of the aortic valve and aortic valve vegetations. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Administration Medical Center.\nAcute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Administration Medical Center.\nA middle-aged man with a history of intravenous drug use who presented with severe myalgias and a petechial rash. He was diagnosed with right-sided staphylococcal endocarditis.\nMitral valve: endocarditis with valve destruction and vegetation. Note the posterior leaflet of the mitral valve, with an irregular vegetation on the atrial surface, resulting in valve destruction at the commissure between the anterior leaflet and the posterior leaflet.\nAortic valve: healed endocarditis. Note the gaping hole with the fibrous rim, and a small strand at the free edge. The hole is at the line of closure. The affected valve is the left cusp. Note the right noncoronary cusp (immediate to the left in this image) demonstrates a small, multichanneled fenestration at the commissure, immediately adjacent to similar fenestrations in the left coronary cusp. These are physiologic lesions occurring with age and are unrelated to endocarditis.\nAortic valve: bicuspid, with infectious endocarditis. In this excised valve, note the bulky vegetations on the ventricular surfaces, with distortion of the valve surfaces.\nMitral valve: postrheumatic, with infectious endocarditis. A defect is seen in the scarred valve, with focal surface hemorrhage. The patient also underwent aortic valve replacement, as there was contiguous infection.\nThe surface of the valves, in most cases, demonstrates areas of acute neutrophilic inflammation with admixed fibrin and platelets. Degenerated bacterial colonies are seen at the left. Also, areas of microcalcification may mimic bacterial deposits.\nInfectious endocarditis, subacute phase. Hemorrhage and prominent granulation tissue with neovascularity is apparent throughout. This aortic valve showed fibrin exudate on the ventricular surface (below), with more prominent organization and granulation on the aortic surface (above).\nInfectious endocarditis, surface of valve leaflet with fibrin; higher magnification of previous image. A chronic infiltrate is seen, just under the denuded thrombosed surface, with primarily macrophages and focal macrophage giant cells.\nBioprosthetic valve with endocarditis. Note the large bacterial colony (staphylococci by culture) in the absence of significant inflammation; the xenograft tissue is not viable, and nuclear detail is not apparent.\nTable 1. Clinical Features of Infective Endocarditis According to Causative Organism\nCausative Organism(s)\nClinical Features of IE\nOverall, S aureus infection is the most common cause of IE, including PVE, acute IE, and IVDA IE.\nApproximately 35-60.5% of staphylococcal bacteremias are complicated by IE.\nMore than half the cases are not associated with underlying valvular disease.\nThe mortality rate of S aureus IE is 40-50%.\nS aureus infection is the second most common cause of nosocomial BSIs, second only to CoNS infection.\nThe incidence of MRSA infections, both the hospital- and community-acquired varieties, has dramatically increased (50% of isolates). Sixty percent of individuals are intermittent carriers of MRSA or MSSA.\nThe primary risk factor for S aureus BSI is the presence of intravascular lines. Other risk factors include cancer, diabetes, corticosteroid use, IVDA, alcoholism, and renal failure.\nThe realization that approximately 50% of hospital- and community-acquired staphylococcal bacteremias arise from infected vascular catheters has led to the reclassification of staphylococcal BSIs. BSIs are acquired not only in the hospital but also in any type of health care facility (eg, nursing home, dialysis center).\nOf S aureus bacteremia cases in the United States, 7.8% (200,000) per year are associated with intravascular catheters.\nStreptococcus viridans\nThis organism accounts for approximately 50-60% of cases of subacute disease.\nMost clinical signs and symptoms are mediated immunologically.\nStreptococcus intermedius group\nThese infections may be acute or subacute.\nS intermedius infection accounts for 15% of streptococcal IE cases.\nMembers of the S intermedius group, especially S anginosus, are unique among the streptococci in that they can actively invade tissue and form abscesses, often in the CNS.\nAbiotrophia\nApproximately 5% of subacute cases of IE are due to infection with Abiotrophia species.\nThey require metabolically active forms of vitamin B-6 for growth.\nThis type of IE is associated with large vegetations that lead to embolization and a high rate of posttreatment relapse.\nGroup D streptococci\nMost cases are subacute.\nThe source is the gastrointestinal or genitourinary tract.\nIt is the third most common cause of IE.\nThey pose major resistance problems for antibiotics.\nNonenterococcal group D\nThe clinical course is subacute.\nInfection often reflects underlying abnormalities of the large bowel (eg, ulcerative colitis, polyps, cancer).\nThe organisms are sensitive to penicillin.\nGroup B streptococci\nAcute disease develops in pregnant patients and older patients with underlying diseases (eg, cancer, diabetes, alcoholism).\nThe mortality rate is 40%.\nComplications include metastatic infection, arterial thrombi, and congestive heart failure.\nIt often requires valve replacement for cure.\nGroup A, C, and G streptococci\nAcute disease resembles that of S aureus IE (30-70% mortality rate), with suppurative complications.\nGroup A organisms respond to penicillin alone.\nGroup C and G organisms require a combination of synergistic antibiotics (as with enterococci).\nCoagulase-negative S aureus\nThis causes subacute disease.\nIt behaves similarly to S viridans infection.\nIt accounts for approximately 30% of PVE cases and less than 5% of NVE cases. [23]\nStaphylococcus lugdunensis\nStaphylococcus lugdunensis is another coagulase-negative Staphylococcus species but is extremely aggressive compared to coagulase-positive S aureus. S lugdunensis frequently causes IE. [24]\nThis is usually acute, except when it involves the right side of the heart in IVDA IE.\nSurgery is commonly required for cure.\nHACEK (ie, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)\nThese organisms usually cause subacute disease.\nThey account for approximately 5% of IE cases.\nThey are the most common gram-negative organisms isolated from patients with IE.\nComplications may include massive arterial emboli and congestive heart failure.\nCure requires ampicillin, gentamicin, and surgery.\nFungal\nThese usually cause subacute disease.\nThe most common organism of both fungal NVE and fungal PVE is Candida albicans.\nFungal IVDA IE is usually caused by Candida parapsilosis or Candida tropicalis.\nAspergillus species are observed in fungal PVE and NIE.\nThe most commonly involved species is Bartonella quintana.\nIE typically develops in homeless males who have extremely substandard hygiene. Bartonella must be considered in cases of culture-negative endocarditis among homeless individuals.\nMultiple pathogens (polymicrobial)\nPseudomonas and enterococci are the most common combination of organisms.\nIt is observed in cases of IVDA IE\nThe cardiac surgery mortality rate is twice that associated with single-agent IE. [25]\nJohn L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance\nJohn L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America\nMichael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London\nMichael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation\nBarry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine\nBarry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine\nSteven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center\nSteven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine\nJon Mark Hirshon, MD, MPH Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine\nJon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine\nThomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine\nThomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society\nKeith A Marill, MD Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor, Harvard Medical School\nKeith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine\nDisclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. 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