Sections

Workup

Approach Considerations

The fundamental standard for diagnosing IE is the documentation of a continuous bacteremia (> 30 min in duration). Although blood cultures remain fundamental in diagnosising 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 often are afebrile and unable to mount a significant fever or exhibit the classic stigmata of valvular infection.

A major clinical challenge is that at least 25% of S aureus BSIs represent IE or metastatic infections. The question is whether a continuous bacteremia in the presence of an intravascular line represents a valvular infection. Blood cultures should be drawn through intravascular lines only for the purpose of diagnosing catheter-related BSIs. Even then, they have limited value.

Because of the ability of S aureus to produce an endotheliosis, the presence of a continuous bacteremia does not necessarily imply an infected valvular vegetation.

An important clue to continuous bacteremia/IE is the presence of S aureus bacteriuria associated with hematuria. Hematuria in the setting of IE results from embolic renal infarction or immunologically mediated glomerulonephritis. Echocardiography has become a useful tool for meeting this clinical challenge.

Twenty-five percent of patients with staphylococcal bacteremia and 23% of those with catheters as the primary focus have evidence of IE on the basis of transesophageal echocardiography (TEE) findings, in the absence of clinical and transthoracic echocardiography (TTE) findings.^[8]

Blood and Urine Studies

Perform baseline studies, such as complete blood count (CBC), electrolytes, creatinine, blood urea nitrogen (BUN), glucose, and coagulation panel, and send to the laboratory for testing.

Anemia is common in subacute endocarditis, and leukocytosis is observed in acute endocarditis. Erythrocyte sedimentation rate (ESR), although not specific, is elevated in more than 90% of cases. Decreased C3, C4, and CH50 are reported in SBE.

Rheumatoid factor (ie, “poor man’s circulating immune complex”) becomes positive in 50% of patients with subacute disease and resolves after successful treatment.

Proteinuria and microscopic hematuria are present in approximately 50% of cases.

Appropriate blood testing for COVID -19 should be performed.

Blood Culture

Patients with PVE or right-sided disease may not have a continuous bacteremia. Five percent to 10% of patients have false-negative blood culture due to recent antibiotic use. Other causes include fastidious organisms and inadequate blood volume; a blood-to-broth ratio of 1:10 is recommended. With modern automated blood culture systems, fastidious organisms such as nutritionally variant streptococci and members of the HACEK group rarely cause culture-negative IE.

As many as 50% of positive blood culture results have been estimated to be falsely positive. This rate probably has decreased, but false-positive blood culture results remain a major diagnostic challenge. One such result can lead to 4 days of unnecessary patient hospitalization.

The significance of positive blood culture results correlates with the following:

The type of organism
The clinical setting (CoNS are significant in patients with prosthetic valves but not in those with native valves.)
Multiple blood cultures positive for the same organism
Shorter incubation time for recovery
The degree of severity of clinical illness

Procedure

Never 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.

The AHA (endorsed by IDSA) guideline update on CIED infections and their management recommends drawing at least 2 sets of blood cultures at evaluation before starting antimicrobial therapy.^[63]

For diagnosing subacute IE, draw 3 to 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.

Using 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.

When blood culture results fail to show an infectious agent after blood is drawn 48 hours after the discontinuation of antibiotic therapy, the second set of blood for cultures should 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 IV lines unless this is part of an approach for diagnosing line infection.^{[78, 79, 80, 81, 82, 83, 84]}

Catheter infection

The 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, 1 sample may be obtained through each of 2 catheter lumens.

In a catheter infection, the colony count of the sample obtained from the suspected port is threefold 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 before their growth is detected in the blood obtained from peripheral vein meets the differential time to positivity criteria of a catheter infection.

A sterile culture of the insertion site has a highly negative predictive value for line infection.^{[79, 80, 81, 82]}

Culture-negative infective endocarditis

Approximately 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.

Culture-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 to 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.

In 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 often are sterile. In S aureus IE, the results of blood cultures may be negative when the organism burrows deep within the thrombus, leaving the surface of the valvular thrombus sterile (surface sterilization).

Valvular 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 usually are sufficient to detect microorganisms in the blood. Additional blood cultures usually are not helpful.

Many 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.

Serology for Chlamydia, Q fever (C burnetii), and Bartonella may be useful in culture-negative endocarditis. Serologic tests often are the most practical means for diagnosing valvular infection with fastidious organisms (eg, C burnetii and Chlamydia, Brucella, and Legionella species).^[78]Buffered charcoal and yeast agar are required for the isolation of Legionella. Brucella species require up to 6 weeks.

It appears that Tropheryma whippelii, which causes Whipple disease, is becoming a more common cause of culture-negative endocarditis. Thuny and colleaguesl^{[46, 85]} 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, a dedicated polymerase chain reaction (PCR) test 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, 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.

Fungal infective endocarditis

Cases of fungal IE often have a low rate of positive blood culture results. Only 50% cases of Candidal blood cultures arepositive. Histoplasma and Aspergillus almost never are retrieved from the bloodstream. Fungal endocarditis always must be considered in the clinical setting of culture-negative IE that fails to respond to appropriate antibiotic therapy.^[86]

Pacemaker infective endocarditis

Establishing 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.

The AHA guideline 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.^{[56, 64, 87]}

The development of the Maldi-Tof allows the ability to identify bacterial or fungal species directly on the culture plates as quickly as they become evident. There is no proven effect on limiting the development of antimicrobial resistance. It does not provide information on the resistance/sensitivity patterns of the detected organisms.

The recent availability of molecular diagnostics such as PCR, multiplex PCR nano particle probes, and PNA Fish allow bypass of the incubation step of traditional culture methods. It does so by identifying organisms specific DNA/RNA directly. It allows multiple targets to be detected from one sample and provides some information on resistance factors inherent in the isolated organisms. Its advantages besides reduced turnaround time are greater accuracy than offered by Maldi-Tof systems as well as providing genetic information regarding sensitivity and resistance patterns. Their limitations include being susceptible to contamination. In polymicrobial cultures, they may not cover all the possible causative pathogens and do not provide phenotypic susceptibility profiles. There is a little data supporting the impact on clinical outcomes or proven effectiveness on limiting the development of antibiotic resistance.^[88]

Echocardiography

Echocardiography 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 never can be excluded on the basis of negative echocardiogram findings, either from transthoracic echocardiography (TTE) or from TEE.

The AHA guideline 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.

Visible vegetation suggests a worse prognosis. Both TTE and TEE are highly specific for valvular vegetations; however, sensitivity differs.

Two-dimensional cardiac Doppler ultrasound testing is 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.

Transthoracic echocardiography is more sensitive for detecting anterior myocardial abscesses and quantitating the degree of valvular dysfunction.

The 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.

The 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.

Conditions 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.

Transthoracic echocardiography generally has had a sensitivity of approximately 60% for identification of valvular lesions in patients with NVE; however, sensitivity was as high as 82% in a recent series where advanced harmonic imaging and digital processing techniques were used.^[83]Transthoracic echcardiography has a sensitivity of only 20% in patients with PVE.

This 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.

View Media Gallery

Transesophageal echocardiography was developed to overcome the problems in visualizing prosthetic valve thrombi and right-sided events. It 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%.

Transesophageal echocardiography 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.

Neither 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.

Echocardiography is useful for predicting the potential complications of IE, especially those that are embolic in nature.

Echocardiographic predictors of systemic embolization in patients with IE are the following:

Large valvular vegetations (>10 mm in diameter)
Multiple vegetations
Mobile but pedunculated vegetations
Noncalcified vegetations
Vegetations that are increasing in size
Prolapsing vegetations

Echocardiography also is highly useful for detecting abscesses. As with valvular lesions, the transesophageal technique is generally more sensitive.^{[89, 90, 91, 92, 93, 94, 95]}

In 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.

In most cases, TTE is sufficient. Transesophageal echocardiography 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 IE cases do not demonstrate any detectable vegetations at the time of the echocardiographic study.

Ultrasonography

Two-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.

Transthoracic echocardiography (TTE) is more sensitive for detecting anterior myocardial abscesses and quantitating the degree of valvular dysfunction.

The 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.

The 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.

Conditions 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.

Radiography

Pulmonary embolic phenomena on radiographs strongly suggest tricuspid disease.

A 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.

View Media Gallery

Multiple embolic pyogenic abscesses may be visualized.

Other Studies

Ventilation/perfusion scanning may be useful in right-sided endocarditis.

Electrocardiography 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.

Catheterization of the heart rarely is 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.

Various radionuclide scans using, for example, gallium (Ga)-67–tagged white cells and indium (In)-111–tagged white cells, are 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.

A computed tomography (CT) scan of the head should be obtained in patients who exhibit central nervous system symptoms or findings consistent with a mass effect (eg, macroabscess of the brain).^[90] This imaging modality has proven most useful for localizing abscesses. With new advanced multislice techniques, CT now can also be used to identify valvular abnormalities and vegetations.^[92]

Evidence increasingly supports the advantages of fluorine-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) scanning over electrocardiographically gated computed tomographic angiography (CTA) in certain circumstances. Positron emission tomography scanning may facilitate earlier diagnoses of infected intracardiac devices and prosthetic valves than do these other studies.

Treatment & Management

John L Brusch MD. infective endocarditis and it’s mimics in the critical care unit. Cunha CB , Cunha BA. inInfectious diseases and antimicrobial stewardship in critical care medicine. Fourth. NY,NY: CRC Press; 2020. Four: 255-263.
Guzek A, Braksator W, Gąsior Z, Kuśmierczyk M, Różański J, Rybicki Z. Infective endocarditis - can we treat it more effectively?. Kardiochir Torakochirurgia Pol. 2020 Mar. 17 (1):8-14. [QxMD MEDLINE Link].
Hackett AJ, Stuart J. Infective endocarditis: identification and management in the emergency department. Emerg Med Pract. 2020 Sep. 22 (9):1-24. [QxMD MEDLINE Link].
Karchmer AW. Infective endocarditis. Harrison’s Principles of Internal Medicine. 16th ed. McGraw-Hill; 2005. 731-40.
Lerner PI, Weinstein L. Infective endocarditis in the antibiotic era. N Engl J Med. 1966 Feb 17. 274(7):388-93 concl. [QxMD MEDLINE Link].
Durack 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. [QxMD MEDLINE Link].
Brusch 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.
Karchmer AW. Infective endocarditis. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. WB Saunders Co; 2005. 1633-1658.
Burke A. Cunha. Diagnostic Reasoning and Clinical Problem Solving. Cheston B. Cunha, Burke A. Cunha. Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine. 4th. Boca Raton: CRC Press; 2020. 3-13.
Peña-Moreno A, Torres-Soblechero L, López-Blázquez M, Butragueño-Laiseca L. Fatal Staphylococcus Aureus Endocarditis Misdiagnosed as Multisystem Inflammatory Syndrome in Children. Pediatr Infect Dis J. 2022 Feb 1. 41 (2):e58-e59. [QxMD MEDLINE Link].
Bajdechi M, Vlad ND, Dumitrascu M, Mocanu E, Dumitru IM, Cernat RC, et al. Bacterial endocarditis masked by COVID-19: A case report. Exp Ther Med. 2022 Feb. 23 (2):186. [QxMD MEDLINE Link].
Hayes DE, Rhee DW, Hisamoto K, Smith D, Ro R, Vainrib AF, et al. Two cases of acute endocarditis misdiagnosed as COVID-19 infection. Echocardiography. 2021 May. 38 (5):798-804. [QxMD MEDLINE Link].
Quintero-Martinez JA, Hindy JR, Mahmood M, Gerberi DJ, DeSimone DC, Baddour LM. A clinical profile of infective endocarditis in patients with recent COVID-19: A systematic review. Am J Med Sci. 2022 Jul. 364 (1):16-22. [QxMD MEDLINE Link].
Demetriades P, Ridley P, Yazdani F, Duckett S. Challenges of remote consultations: a delayed diagnosis of aortic valve endocarditis complicated by recurrent intracranial events. BMJ Case Rep. 2022 Feb 28. 15 (2):[QxMD MEDLINE Link].
George A, Alampoondi Venkataramanan SV, John KJ, Mishra AK. Infective endocarditis and COVID -19 coinfection: An updated review. Acta Biomed. 2022 Mar 14. 93 (1):e2022030. [QxMD MEDLINE Link].
Clerc O, Prod'hom G, Senn L, Jaton K, Zanetti G, Calandra T, et al. Matrix-assisted laser desorption ionization time-of-flight mass spectrometry and PCR-based rapid diagnosis of Staphylococcus aureus bacteraemia. Clin Microbiol Infect. 2014 Apr. 20 (4):355-60. [QxMD MEDLINE Link].
El-Dalati S, Cronin D, Riddell J 4th, Shea M, Weinberg RL, Stoneman E, et al. A step-by-step guide to implementing a multidisciplinary endocarditis team. Ther Adv Infect Dis. 2021 Jan-Dec. 8:20499361211065596. [QxMD MEDLINE Link].
Rawson TM, Hernandez B, Moore LSP, Herrero P, Charani E, Ming D, et al. A Real-world Evaluation of a Case-based Reasoning Algorithm to Support Antimicrobial Prescribing Decisions in Acute Care. Clin Infect Dis. 2021 Jun 15. 72 (12):2103-2111. [QxMD MEDLINE Link].
Lerner PI, Weinstein L. Infective endocarditis in the antibiotic era. N Engl J Med. 1966 Feb 3. 274(5):259-66 contd. [QxMD MEDLINE Link].
Lerner PI, Weinstein L. Infective endocarditis in the antibiotic era. N Engl J Med. 1966 Jan 27. 274(4):199-206 contd. [QxMD MEDLINE Link].
Brusch J. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007.
Cahill TJ, Baddour LM, Habib G, Hoen B, Salaun E, Pettersson GB, et al. Challenges in Infective Endocarditis. J Am Coll Cardiol. 2017 Jan 24. 69 (3):325-344. [QxMD MEDLINE Link].
Weinstein LW, Brusch JL. Infective Endocarditis. New York, NY: Oxford University Press; 1996.
Wang A, Athan E, Pappas PA, Fowler VG Jr, Olaison L, Paré C, et al. Contemporary clinical profile and outcome of prosthetic valve endocarditis. JAMA. 2007 Mar 28. 297(12):1354-61. [QxMD MEDLINE Link].
Miró JM, del Río A, Mestres CA. Infective endocarditis in intravenous drug abusers and HIV-1 infected patients. Infect Dis Clin North Am. 2002 Jun. 16(2):273-95, vii-viii. [QxMD MEDLINE Link].
Schranz AJ, Fleischauer A, Chu VH, Wu LT, Rosen DL. Trends in Drug Use-Associated Infective Endocarditis and Heart Valve Surgery, 2007 to 2017: A Study of Statewide Discharge Data. Ann Intern Med. 2018 Dec 4. [QxMD MEDLINE Link].
Soong G, Chun J, Parker D, Prince A. Staphylococcus aureus activation of caspase 1/calpain signaling mediates invasion through human keratinocytes. J Infect Dis. 2012 May 15. 205(10):1571-9. [QxMD MEDLINE Link]. [Full Text].
Snygg-Martin U, Giang KW, Dellborg M, Robertson J, Mandalenakis Z. Cumulative Incidence of Infective Endocarditis in Patients with Congenital Heart Disease: A Nationwide, Case-Control Study Over Nine Decades. Clin Infect Dis. 2021 Oct 20. 73 (8):1469-1475. [QxMD MEDLINE Link].
Xiong YQ, Fowler VG, Yeaman MR, Perdreau-Remington F, Kreiswirth BN, Bayer AS. Phenotypic and genotypic characteristics of persistent methicillin-resistant Staphylococcus aureus bacteremia in vitro and in an experimental endocarditis model. J Infect Dis. 2009 Jan 15. 199(2):201-8. [QxMD MEDLINE Link]. [Full Text].
Chu VH, Miro JM, Hoen B, Cabell CH, Pappas PA, Jones P, et al. Coagulase-negative staphylococcal prosthetic valve endocarditis--a contemporary update based on the International Collaboration on Endocarditis: prospective cohort study. Heart. 2009 Apr. 95(7):570-6. [QxMD MEDLINE Link].
Reyes MP, Ali A, Mendes RE, Biedenbach DJ. Resurgence of Pseudomonas endocarditis in Detroit, 2006-2008. Medicine (Baltimore). 2009 Sep. 88(5):294-301. [QxMD MEDLINE Link].
Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG Jr, Bayer AS, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009 Mar 9. 169(5):463-73. [QxMD MEDLINE Link].
Baddour LM, Cha YM, Wilson WR. Clinical practice. Infections of cardiovascular implantable electronic devices. N Engl J Med. 2012 Aug 30. 367(9):842-9. [QxMD MEDLINE Link].
Baddley JW, Benjamin DK Jr, Patel M, Miró J, Athan E, Barsic B, et al. Candida infective endocarditis. Eur J Clin Microbiol Infect Dis. 2008 Jul. 27(7):519-29. [QxMD MEDLINE Link]. [Full Text].
Chu VH, Woods CW, Miro JM, Hoen B, Cabell CH, Pappas PA, et al. Emergence of coagulase-negative staphylococci as a cause of native valve endocarditis. Clin Infect Dis. 2008 Jan 15. 46(2):232-42. [QxMD MEDLINE Link].
Liu PY, Huang YF, Tang CW, Chen YY, Hsieh KS, Ger LP, et al. Staphylococcus lugdunensis infective endocarditis: a literature review and analysis of risk factors. J Microbiol Immunol Infect. 2010 Dec. 43 (6):478-84. [QxMD MEDLINE Link].
Hill EE, Herijgers P, Claus P, Vanderschueren S, Herregods MC, Peetermans WE. Infective endocarditis: changing epidemiology and predictors of 6-month mortality: a prospective cohort study. Eur Heart J. 2007 Jan. 28(2):196-203. [QxMD MEDLINE Link].
Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med. 2001 Nov 1. 345(18):1318-30. [QxMD MEDLINE Link].
Bor DH, Woolhandler S, Nardin R, Brusch J, Himmelstein DU. Infective endocarditis in the u.s., 1998-2009: a nationwide study. PLoS One. 2013. 8(3):e60033. [QxMD MEDLINE Link]. [Full Text].
Tleyjeh IM, Steckelberg JM, Murad HS, Anavekar NS, Ghomrawi HM, Mirzoyev Z, et al. Temporal trends in infective endocarditis: a population-based study in Olmsted County, Minnesota. JAMA. 2005 Jun 22. 293(24):3022-8. [QxMD MEDLINE Link].
Mendiratta P, Tilford JM, Prodhan P, Cleves MA, Wei JY. Trends in hospital discharge disposition for elderly patients with infective endocarditis: 1993 to 2003. J Am Geriatr Soc. 2009 May. 57(5):877-81. [QxMD MEDLINE Link].
Kiefer T, Park L, Tribouilloy C, Cortes C, Casillo R, Chu V, et al. Association between valvular surgery and mortality among patients with infective endocarditis complicated by heart failure. JAMA. 2011 Nov 23. 306(20):2239-47. [QxMD MEDLINE Link].
Ortiz-Bautista C, López J, García-Granja PE, Vilacosta I, Sevilla T, Sarriá C, et al. Right-sided infective endocarditis in cardiac device carriers: Clinical profile and prognosis. Med Clin (Barc). 2017 Jun 22. [QxMD MEDLINE Link].
Sonneville R, Mirabel M, Hajage D, et al. Neurologic complications and outcomes of infective endocarditis in critically ill patients: The ENDOcardite en REAnimation prospective multicenter study. Crit Care Med. 2011 Jun. 39(6):1474-1481. [QxMD MEDLINE Link].
Kang DH, Kim YJ, Kim SH, et al. Early surgery versus conventional treatment for infective endocarditis. N Engl J Med. 2012 Jun 28. 366(26):2466-73. [QxMD MEDLINE Link].
Thuny F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. Lancet. 2012 Mar 10. 379(9819):965-75. [QxMD MEDLINE Link].
Wallace SM, Walton BI, Kharbanda RK, Hardy R, Wilson AP, Swanton RH. Mortality from infective endocarditis: clinical predictors of outcome. Heart. 2002 Jul. 88(1):53-60. [QxMD MEDLINE Link]. [Full Text].
Durante-Mangoni E, Bradley S, Selton-Suty C, Tripodi MF, Barsic B, Bouza E, et al. Current features of infective endocarditis in elderly patients: results of the International Collaboration on Endocarditis Prospective Cohort Study. Arch Intern Med. 2008 Oct 27. 168(19):2095-103. [QxMD MEDLINE Link].
Chu VH, Cabell CH, Benjamin DK Jr, Kuniholm EF, Fowler VG Jr, Engemann J, et al. Early predictors of in-hospital death in infective endocarditis. Circulation. 2004 Apr 13. 109(14):1745-9. [QxMD MEDLINE Link].
[Guideline] National Institute for Health and Clinical Excellence. Prophylaxis against infective endocarditis. Antimicrobial prophylaxis against infective endocarditis in adults and children undergoing interventional procedures. 2008. (NICE clinical guideline No. 64).
Özcan C, Raunsø J, Lamberts M, Køber L, Lindhardt TB, Bruun NE, et al. Infective endocarditis and risk of death after cardiac implantable electronic device implantation: a nationwide cohort study. Europace. 2017 Jan 10. [QxMD MEDLINE Link].
Cresti A, Chiavarelli M, Scalese M, Nencioni C, Valentini S, Guerrini F, et al. Epidemiological and mortality trends in infective endocarditis, a 17-year population-based prospective study. Cardiovasc Diagn Ther. 2017 Feb. 7 (1):27-35. [QxMD MEDLINE Link].
Janga KC, Sinha A, Greenberg S, Sharma K. Nephrologists Hate the Dialysis Catheters: A Systemic Review of Dialysis Catheter Associated Infective Endocarditis. Case Rep Nephrol. 2017. 2017:9460671. [QxMD MEDLINE Link].
[Guideline] Baddour LM, Epstein AE, Erickson CC, et al. Update on cardiovascular implantable electronic device infections and their management: a scientific statement from the American Heart Association. Circulation. 2010 Jan 26. 121(3):458-77. [QxMD MEDLINE Link].
Crawford MH, Durack DT. Clinical presentation of infective endocarditis. Cardiol Clin. 2003 May. 21(2):159-66, v. [QxMD MEDLINE Link].
Di Salvo G, Habib G, Pergola V, Avierinos JF, Philip E, Casalta JP, et al. Echocardiography predicts embolic events in infective endocarditis. J Am Coll Cardiol. 2001 Mar 15. 37(4):1069-76. [QxMD MEDLINE Link].
Eknoyan G, Lister BJ, Kim HS, Greenberg SD. Renal complications of bacterial endocarditis. Am J Nephrol. 1985. 5(6):457-69. [QxMD MEDLINE Link].
Pruitt AA, Rubin RH, Karchmer AW, Duncan GW. Neurologic complications of bacterial endocarditis. Medicine (Baltimore). 1978 Jul. 57(4):329-43. [QxMD MEDLINE Link].
Bajdechi M, Vlad ND, Dumitrascu M, Mocanu E, Dumitru IM, Cernat RC, et al. Bacterial endocarditis masked by COVID-19: A case report. Exp Ther Med. 2022 Feb. 23 (2):186. [QxMD MEDLINE Link].
Blagova OV, Kogan EA, Lutokhina YA, Kukleva AD, Ainetdinova DH, Novosadov VM, et al. Subacute and chronic post-covid myoendocarditis: clinical presentation, role of coronavirus persistence and autoimmune mechanisms. Kardiologiia. 2021 Jul 1. 61 (6):11-27. [QxMD MEDLINE Link].
[Guideline] Sexton DJ, Spelman D. Current best practices and guidelines. Assessment and management of complications in infective endocarditis. Cardiol Clin. 2003 May. 21(2):273-82, vii-viii. [QxMD MEDLINE Link].
George A, Alampoondi Venkataramanan SV, John KJ, Mishra AK. Infective endocarditis and COVID -19 coinfection: An updated review. Acta Biomed. 2022 Mar 14. 93 (1):e2022030. [QxMD MEDLINE Link].
Snygg-Martin U, Gustafsson L, Rosengren L, Alsiö A, Ackerholm P, Andersson R, et al. Cerebrovascular complications in patients with left-sided infective endocarditis are common: a prospective study using magnetic resonance imaging and neurochemical brain damage markers. Clin Infect Dis. 2008 Jul 1. 47(1):23-30. [QxMD MEDLINE Link].
Terpenning MS, Buggy BP, Kauffman CA. Infective endocarditis: clinical features in young and elderly patients. Am J Med. 1987 Oct. 83(4):626-34. [QxMD MEDLINE Link].
Bansal RC. Infective endocarditis. Med Clin North Am. 1995 Sep. 79(5):1205-40. [QxMD MEDLINE Link].
Conlon PJ, Jefferies F, Krigman HR, Corey GR, Sexton DJ, Abramson MA. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol. 1998 Feb. 49(2):96-101. [QxMD MEDLINE Link].
Cosmi JE, Tunick PA, Kronzon I. Mortality in patients with paravalvular abscess diagnosed by transesophageal echocardiography. J Am Soc Echocardiogr. 2004 Jul. 17(7):766-8. [QxMD MEDLINE Link].
Fowler VG Jr, Scheld WM, Bayer AS. Endocarditis and intravascular infections. Mandell GL, Bennett JA, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, Penn: Elseiver; 2005. 975-1021.
Cunha BA, Gill MV, Lazar JM. Acute infective endocarditis. Diagnostic and therapeutic approach. Infect Dis Clin North Am. 1996 Dec. 10(4):811-34. [QxMD MEDLINE Link].
Roberts NK, Somerville J. Pathological significance of electrocardiographic changes in aortic valve endocarditis. Br Heart J. 1969 May. 31(3):395-6. [QxMD MEDLINE Link].
Robinson SL, Saxe JM, Lucas CE, Arbulu A, Ledgerwood AM, Lucas WF. Splenic abscess associated with endocarditis. Surgery. 1992 Oct. 112(4):781-6; discussion 786-7. [QxMD MEDLINE Link].
Weinstein L. Life-threatening complications of infective endocarditis and their management. Arch Intern Med. 1986 May. 146(5):953-7. [QxMD MEDLINE Link].
Weinstein L, Schlesinger JJ. Pathoanatomic, pathophysiologic and clinical correlations in endocarditis (first of two parts). N Engl J Med. 1974 Oct 17. 291(16):832-7. [QxMD MEDLINE Link].
Wang CC, Lee CH, Chan CY, Chen HW. Splenic infarction and abscess complicating infective endocarditis. Am J Emerg Med. 2009 Oct. 27(8):1021.e3-5. [QxMD MEDLINE Link].
Kradin RL. Pathology of infective endocarditis. Brusch JL, ed. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007. 101-18.
Brusch JL. Pathoanatomical, pathophysiological and clinical correlations. Brusch JL, ed. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007. 119-41.
Quintero-Martinez JA, Hindy JR, Mahmood M, Gerberi DJ, DeSimone DC, Baddour LM. A clinical profile of infective endocarditis in patients with recent COVID-19: A systematic review. Am J Med Sci. 2022 Jul. 364 (1):16-22. [QxMD MEDLINE Link].
Khatib R, Riederer K, Saeed S, Johnson LB, Fakih MG, Sharma M, et al. Time to positivity in Staphylococcus aureus bacteremia: possible correlation with the source and outcome of infection. Clin Infect Dis. 2005 Sep 1. 41(5):594-8. [QxMD MEDLINE Link].
Lee A, Mirrett S, Reller LB, Weinstein MP. Detection of bloodstream infections in adults: how many blood cultures are needed?. J Clin Microbiol. 2007 Nov. 45(11):3546-8. [QxMD MEDLINE Link]. [Full Text].
[Guideline] Mermel LA, Allon M, Bouza E, Craven DE, Flynn P, O'Grady NP, et al. Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2009 Jul 1. 49(1):1-45. [QxMD MEDLINE Link].
Weinbaum FI, Lavie S, Danek M, Sixsmith D, Heinrich GF, Mills SS. Doing it right the first time: quality improvement and the contaminant blood culture. J Clin Microbiol. 1997 Mar. 35(3):563-5. [QxMD MEDLINE Link]. [Full Text].
Weinstein MP. Blood culture contamination: persisting problems and partial progress. J Clin Microbiol. 2003 Jun. 41(6):2275-8. [QxMD MEDLINE Link]. [Full Text].
Casella F, Rana B, Casazza G, Bhan A, Kapetanakis S, Omigie J, et al. The potential impact of contemporary transthoracic echocardiography on the management of patients with native valve endocarditis: a comparison with transesophageal echocardiography. Echocardiography. 2009 Sep. 26(8):900-6. [QxMD MEDLINE Link].
Choussat R, Thomas D, Isnard R, Michel PL, Iung B, Hanania G, et al. Perivalvular abscesses associated with endocarditis; clinical features and prognostic factors of overall survival in a series of 233 cases. Perivalvular Abscesses French Multicentre Study. Eur Heart J. 1999 Feb. 20(3):232-41. [QxMD MEDLINE Link].
Bates DW, Goldman L, Lee TH. Contaminant blood cultures and resource utilization. The true consequences of false-positive results. JAMA. 1991 Jan 16. 265(3):365-9. [QxMD MEDLINE Link].
Falagas ME, Manta KG, Ntziora F, Vardakas KZ. Linezolid for the treatment of patients with endocarditis: a systematic review of the published evidence. J Antimicrob Chemother. 2006 Aug. 58(2):273-80. [QxMD MEDLINE Link].
Sridhar AR, Lavu M, Yarlagadda V, Reddy M, Gunda S, Afzal R, et al. Cardiac Implantable Electronic Device-Related Infection and Extraction Trends in the U.S. Pacing Clin Electrophysiol. 2017 Mar. 40 (3):286-293. [QxMD MEDLINE Link].
Buchan BW, Windham S, Balada-Llasat JM, Leber A, et al. Practical Comparison of the BioFire FilmArray Pneumonia Panel to Routine Diagnostic Methods and Potential Impact on Antimicrobial Stewardship in Adult Hospitalized Patients with Lower Respiratory Tract Infections. J Clin Microbiol. 2020 Jun 24. 58 (7):[QxMD MEDLINE Link].
[Guideline] Cheitlin MD, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ, Davis JL, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation. 2003 Sep 2. 108(9):1146-62. [QxMD MEDLINE Link].
Jassal DS, Picard MH. Echocardiography. Brusch JL, ed. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007. 255-72.
Roe MT, Abramson MA, Li J, Heinle SK, Kisslo J, Corey GR, et al. Clinical information determines the impact of transesophageal echocardiography on the diagnosis of infective endocarditis by the duke criteria. Am Heart J. 2000 Jun. 139(6):945-51. [QxMD MEDLINE Link].
Feuchtner GM, Stolzmann P, Dichtl W, Schertler T, Bonatti J, Scheffel H, et al. Multislice computed tomography in infective endocarditis: comparison with transesophageal echocardiography and intraoperative findings. J Am Coll Cardiol. 2009 Feb 3. 53(5):436-44. [QxMD MEDLINE Link].
Chen W, Sajadi MM, Dilsizian V. Merits of FDG PET/CT and Functional Molecular Imaging Over Anatomic Imaging With Echocardiography and CT Angiography for the Diagnosis of Cardiac Device Infections. JACC Cardiovasc Imaging. 2018 Nov. 11 (11):1679-1691. [QxMD MEDLINE Link].
Fowler VG Jr, Boucher HW, Corey GR, Abrutyn E, Karchmer AW, Rupp ME, et al. Daptomycin versus standard therapy for bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. 2006 Aug 17. 355(7):653-65. [QxMD MEDLINE Link].
Iversen K, Ihlemann N, Gill SU, Madsen T, Elming H, Jensen KT, et al. Partial Oral versus Intravenous Antibiotic Treatment of Endocarditis. N Engl J Med. 2018 Aug 28. [QxMD MEDLINE Link].
Cunha BA. Persistent S. aureus acute bacteremia: clinical pathway for diagnosis and treatment. Antibiot for Clin. 2006. 10:39-46.
Pujol M, Miró JM, Shaw E, Aguado JM, et al. Daptomycin Plus Fosfomycin Versus Daptomycin Alone for Methicillin-resistant Staphylococcus aureus Bacteremia and Endocarditis: A Randomized Clinical Trial. Clin Infect Dis. 2021 May 4. 72 (9):1517-1525. [QxMD MEDLINE Link].
Buckholz 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.
Jones T, Yeaman MR, Sakoulas G, Yang SJ, Proctor RA, Sahl HG, et al. Failures in clinical treatment of Staphylococcus aureus Infection with daptomycin are associated with alterations in surface charge, membrane phospholipid asymmetry, and drug binding. Antimicrob Agents Chemother. 2008 Jan. 52(1):269-78. [QxMD MEDLINE Link]. [Full Text].
Sakoulas G, Moise-Broder PA, Schentag J, Forrest A, Moellering RC Jr, Eliopoulos GM. Relationship of MIC and bactericidal activity to efficacy of vancomycin for treatment of methicillin-resistant Staphylococcus aureus bacteremia. J Clin Microbiol. 2004 Jun. 42(6):2398-402. [QxMD MEDLINE Link]. [Full Text].
Pronovost P, Needham D, Berenholtz S, Sinopoli D, Chu H, Cosgrove S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med. 2006 Dec 28. 355(26):2725-32. [QxMD MEDLINE Link].
Bailey J, Summers KM. Dalbavancin: a new lipoglycopeptide antibiotic. Am J Health Syst Pharm. 2008 Apr 1. 65 (7):599-610. [QxMD MEDLINE Link].
Kaasch AJ, Jung N. Editorial Commentary: Transesophageal Echocardiography in Staphylococcus aureus Bloodstream Infection--Always Needed?. Clin Infect Dis. 2015 Jul 1. 61 (1):29-30. [QxMD MEDLINE Link].
Fowler VG Jr, Li J, Corey GR, Boley J, Marr KA, Gopal AK, et al. Role of echocardiography in evaluation of patients with Staphylococcus aureus bacteremia: experience in 103 patients. J Am Coll Cardiol. 1997 Oct. 30(4):1072-8. [QxMD MEDLINE Link].
Fowler VG Jr, Miro JM, Hoen B, Cabell CH, Abrutyn E, Rubinstein E, et al. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2005 Jun 22. 293(24):3012-21. [QxMD MEDLINE Link].
Khatib R, Johnson LB, Fakih MG, Riederer K, Khosrovaneh A, Shamse Tabriz M, et al. Persistence in Staphylococcus aureus bacteremia: incidence, characteristics of patients and outcome. Scand J Infect Dis. 2006. 38(1):7-14. [QxMD MEDLINE Link].
Duval X, Selton-Suty C, Alla F, Salvador-Mazenq M, Bernard Y, Weber M, et al. Endocarditis in patients with a permanent pacemaker: a 1-year epidemiological survey on infective endocarditis due to valvular and/or pacemaker infection. Clin Infect Dis. 2004 Jul 1. 39(1):68-74. [QxMD MEDLINE Link].
[Guideline] Olaison L, Pettersson G. Current best practices and guidelines indications for surgical intervention in infective endocarditis. Infect Dis Clin North Am. 2002 Jun. 16(2):453-75, xi. [QxMD MEDLINE Link].
Sławiński G, Lewicka E, Kempa M, Budrejko S, Raczak G. Infections of cardiac implantable electronic devices: Epidemiology, classification, treatment, and prognosis. Adv Clin Exp Med. 2018 Jul 26. [QxMD MEDLINE Link].
[Guideline] Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9. 116(15):1736-54. [QxMD MEDLINE Link].
Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA. 1997 Jun 11. 277(22):1794-801. [QxMD MEDLINE Link].
Bach DS. Perspectives on the American College of Cardiology/American Heart Association guidelines for the prevention of infective endocarditis. J Am Coll Cardiol. 2009 May 19. 53(20):1852-4. [QxMD MEDLINE Link].
Thornhill MH, Dayer MJ, Forde JM, et al. Impact of the NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and after study. BMJ. 2011 May 3. 342:d2392. [QxMD MEDLINE Link]. [Full Text].
Baddour LM, Wilson LM. Infections of prosthetic valves and other cardiovascular devices: intravascular devices. Mandell GL, Bennett JE, Dolin R, eds. Mandel, Douglas and Bennett’s Principles and Practice and Infectious Diseases. 5th ed. Philadelphia, Pa: Elsevier; 2005. 1022-44.
Slipczuk L, Codolosa JN, Davila CD, Romero-Corral A, Yun J, Pressman GS, et al. Infective endocarditis epidemiology over five decades: a systematic review. PLoS One. 2013. 8 (12):e82665. [QxMD MEDLINE Link].
[Guideline] Towns ML, Reller LB. Diagnostic methods current best practices and guidelines for isolation of bacteria and fungi in infective endocarditis. Infect Dis Clin North Am. 2002 Jun. 16(2):363-76, ix-x. [QxMD MEDLINE Link].
Brusch JL. Legionnaire's Disease: Cardiac Manifestations. Infect Dis Clin North Am. 2017 Mar. 31 (1):69-80. [QxMD MEDLINE Link].
Thuny F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. Lancet. 2012 Mar 10. 379(9819):965-75. [QxMD MEDLINE Link].
Thornhill MH, Gibson TB, Cutler E, Dayer MJ, Chu VH, Lockhart PB, et al. Antibiotic Prophylaxis and Incidence of Endocarditis Before and After the 2007 AHA Recommendations. J Am Coll Cardiol. 2018 Nov 13. 72 (20):2443-2454. [QxMD MEDLINE Link].
Janszky I, Gémes K, Ahnve S, Asgeirsson H, Möller J. Invasive Procedures Associated With the Development of Infective Endocarditis. J Am Coll Cardiol. 2018 Jun 19. 71 (24):2744-2752. [QxMD MEDLINE Link].
Forsblom E, Ruotsalainen E, Ollgren J, Järvinen A. Telephone consultation cannot replace bedside infectious disease consultation in the management of Staphylococcus aureus Bacteremia. Clin Infect Dis. 2013 Feb. 56 (4):527-35. [QxMD MEDLINE Link].
Nishimura 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.
Netzer 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. [QxMD MEDLINE Link]. [Full Text].
[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. [QxMD MEDLINE Link].
Weber C, Luehr M, Petrov G, Misfeld M, et al. Impact of the 2009 ESC Guideline Change on Surgically Treated Infective Endocarditis. Ann Thorac Surg. 2022 Feb 22. [QxMD MEDLINE Link].
Wilson WR, Gewitz M, Lockhart PB, Bolger AF, et al. Adapted from: Prevention of Viridans Group Streptococcal Infective Endocarditis: A Scientific Statement From the American Heart Association. J Am Dent Assoc. 2021 Nov. 152 (11):886-902.e2. [QxMD MEDLINE Link].
Tarakji,kg. bacterial envelope to prevent cardiac implantable device infections. new england J Med. may 16 2019. 380:3895.
Archibald LK, Pallangyo K, Kazembe P, Reller LB. Blood culture contamination in Tanzania, Malawi, and the United States: a microbiological tale of three cities. J Clin Microbiol. 2006 Dec. 44(12):4425-9. [QxMD MEDLINE Link]. [Full Text].
Correction to: Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. 2016 Aug 23. 134 (8):e113. [QxMD MEDLINE Link].
Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Bolger AF, Levison ME, et al. 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. [QxMD MEDLINE Link].
George A, Alampoondi Venkataramanan SV, John KJ, Mishra AK. Infective endocarditis and COVID -19 coinfection: An updated review. Acta Biomed. 2022 Mar 14. 93 (1):e2022030. [QxMD MEDLINE Link].
JL Brusch. Endocarditis. Cheston B. Cunha. Schlossberg's Clinical Infectious Disease. 3rd. Oxford University Press; 18 February 2022. 243-254.

Media Gallery

Acute 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 Affairs Medical Center.
Acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Affairs Medical Center.
A 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.
This 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.
A 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.
Mitral 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.
Aortic 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.
Aortic valve: bicuspid, with infectious endocarditis. In this excised valve, note the bulky vegetations on the ventricular surfaces, with distortion of the valve surfaces.
Mitral 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.
The 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.
Infectious 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).
Infectious 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.
Bioprosthetic 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.

of 13

Table 1. Clinical Features of Infective Endocarditis According to Causative Organism

Causative Organism(s)	Clinical Features of IE
Staphylococcus aureus	Overall, S aureus infection is the most common cause of IE, including PVE, acute IE, and IVDA IE. Approximately 35-60.5% of staphylococcal bacteremias are complicated by IE. More than half of cases are not associated with underlying valvular disease. The mortality rate for S aureus IE is 40-50%. Staphylococcus aureus infection is the second most common cause of nosocomial BSIs, second only to CoNS infection. The 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. The 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. The 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 carried not only in the hospital but also in any type of healthcare facility (eg, nursing home, dialysis center). Of S aureus bacteremia cases in the United States, 7.8% (200,000) per year are associated with intravascular catheters.
Streptococcus viridans	This organism accounts for approximately 50-60% of cases of subacute disease. Most clinical signs and symptoms are mediated immunologically.
Streptococcus intermedius group	These infections may be acute or subacute. Streptococcus intermedius infection accounts for 15% of streptococcal IE cases. Members 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.
Abiotrophia	Approximately 5% of subacute cases of IE are due to infection with Abiotrophia species. They require metabolically active forms of vitamin B-6 for growth. This type of IE is associated with large vegetations that lead to embolization and a high rate of posttreatment relapse.
Group D streptococci	Most cases are subacute. The source is the gastrointestinal or genitourinary tract. It is the third most common cause of IE. They pose major resistance problems for antibiotics.
Nonenterococcal group D	The clinical course is subacute. Infection often reflects underlying abnormalities of the large bowel (eg, ulcerative colitis, polyps, cancer). The organisms are sensitive to penicillin.
Group B streptococci	Acute disease develops in pregnant patients and older patients with underlying diseases (eg, cancer, diabetes, alcoholism). The mortality rate is 40%. Complications include metastatic infection, arterial thrombi, and congestive heart failure. It often requires valve replacement for cure.
Group A, C, and G streptococci	Acute disease resembles that of S aureus IE (30-70% mortality rate), with suppurative complications. Group A organisms respond to penicillin alone. Group C and G organisms require a combination of synergistic antibiotics (as with enterococci).
Coagulase-negative S aureus	This causes subacute disease. It behaves similarly to S viridans infection. It accounts for approximately 30% of PVE cases and less than 5% of NVE cases.^[36]
Staphylococcus lugdunensis	Staphylococcus lugdunensis is another coagulase-negative Staphylococcus species but is extremely aggressive compared to coagulase-positive S aureus. S lugdunensis frequently causes IE. ^[37]
Pseudomonas aeruginosa	This is usually acute, except when it involves the right side of the heart in IVDA IE. Surgery is commonly required for cure.
HACEK (ie, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)	These organisms usually cause subacute disease. They account for approximately 5% of IE cases. They are the most common gram-negative organisms isolated from patients with IE. Complications may include massive arterial emboli and congestive heart failure. Cure requires ampicillin, gentamicin, and surgery.
Fungal	These usually cause subacute disease. The most common organism of both fungal NVE and fungal PVE is Candida albicans. Fungal IVDA IE is usually caused by Candida parapsilosis or Candida tropicalis. Aspergillus species are observed in fungal PVE and NIE.
Bartonella	The most commonly involved species is Bartonella quintana. Infective endocarditis typically develops in homeless males who have extremely substandard hygiene. Bartonella must be considered in cases of culture-negative endocarditis among homeless individuals.
Multiple pathogens (polymicrobial)	Pseudomonas and enterococci are the most common combination of organisms. It is observed in cases of IVDA IE The cardiac surgery mortality rate is twice that associated with single-agent IE.^[37]