Guidelines Summary

Key points of the American Heart Association's guidelines for the treatment of IE in adults are summarized below.^[103]

Definition

The diagnosis of IE should be based on syndromic reasoning and includes pathologic criteria and clinical criteria. The diagnosis is differentiated as definite, possible, or rejected IE.

Blood cultures

Blood cultures should be collected at least 3 times from different venipuncture sites. The first and second collections should be taken at least 1 hour apart.

Echocardiography

Transthoracic echocardiography (TTE) should be performed as quickly as possible in all cases of suspected IE. If the initial TTE images are inadequate, or if findings are negative in the setting of persistent suspicion for IE, transesophageal echocardiography (TEE) should be performed. Transesophageal echocardiography also should be performed in patients with possible intracardiac complications in whom TTE findings were initially positive. If the suspicion for IE remains high despite negative TEE findings, a repeat TEE should be performed after 3 to 5 days. Furthermore, repeat TEE should be performed if a new intracardiac complication is suggested by clinical features. Performance of TTE also is reasonable upon completion of antibiotic therapy for the establishment of a new baseline.

Surgical intervention

Especially in challenging cases, as below, in which surgery is considered, the therapeutic approach should be arrived at by a team consisting of infectious disease specialist, cardiologist, and cardiac surgeon. In cases of opioid use disorder (OUD), there should be input of a substance abuse specialist and medical ethicist because of the high rate of recidivism in this group of patients.

The following features may merit surgical intervention:

Persistent vegetation following systemic embolization
Anterior mitral leaflet vegetation, especially larger than 10 mm
One or more embolic events during the first 14 days of antimicrobial therapy
Growing vegetation despite appropriate antimicrobial therapy
Acute mitral or aortic regurgitation with signs of heart failure
Heart failure that does not respond to medical therapy
Paravalvular extension
Valvular dehiscence, rupture, or fistula formation
New heart block
Large abscess or extension of abscess despite appropriate antimicrobial therapy

Antimicrobial therapy

The guidelines make specific recommendations for the following:

Native valve IE caused by highly susceptible (MIC ≤0.12 µg/mL) viridans group streptococci (VGS)
Viridans group streptococci and S bovis with MIC >0.12 µg/mL to < 0.5 µg/mL
Abiotrophia defectiva and Granulicatella species, and VGS with penicillin MIC ≥0.5 µg/mL
Viridans group streptococci or S bovis infection of prosthetic material
Staphylococcal infection
Staphylococcal infection of prosthetic material
Enterococcal infection
Infection with HACEK micro-organisms
Infection with non-HACEK gram-negative bacilli
Culture-negative endocarditis
Fungal infection
Early surgery for native valve IE

The following scenarios support early valve surgery for native left-sided IE:

Signs or symptoms of heart failure as a result of valve dysfunction
IE caused by fungal infection or highly resistant organisms
IE complicated by annular abscess, heart block, or destructive perforating lesions
Persistent infection (bacteremia or fever; >5-7 days) after appropriate antimicrobial therapy has been initiated, if other sources of fever or infection have been ruled out
Recurrent emboli or persistent/growing vegetations despite appropriate antimicrobial therapy

Early surgery (prosthetic valve IE)

The following scenarios support the consideration of early valve surgery for prosthetic valve IE:

Signs or symptoms of heart failure resulting from intracardiac fistula, valve dehiscence, or severe prosthetic dysfunction
Persistent bacteremia (>5-7 days) after the start of appropriate antimicrobial therapy
Prosthetic valve IE complicated by annular abscess, heart block, or destructive perforating lesions
Prosthetic valve IE caused by fungal infection or highly resistant organisms
Recurrent emboli despite appropriate antimicrobial therapy

Anticoagulation

It is reasonable to discontinue all forms of anticoagulation for 2 weeks in patients with a mechanical valve and IE in whom a CNS embolic event has occurred. Antiplatelet therapy should not be initiated as adjunctive therapy upon a diagnosis of IE, although established antiplatelet therapy may be continued in patients with IE who have no bleeding complications.

CNS imaging

CNS imaging should be performed to evaluate for CNS bleeding or intracranial mycotic aneurysm in patients with IE with neurological deficits, severe localized headache, or meningeal signs.

Medication

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[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].
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Tarakji,kg. bacterial envelope to prevent cardiac implantable device infections. new england J Med. may 16 2019. 380:3895.

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.

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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. S gordonii has migrated from Norway to the United States over the last 15 years. It characteristically is associated with a sterile inflammatory response manifest after the bacterial component has been successfully treated.
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 ₆for 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.
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.
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. Candida auris is progressively contaminating all types of healthcare facilities worldwide
Bartonella	The most 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.

Table 2. Differential Diagnoses of IE During the COVID-19 Pandemic

COVID-19 infection with or without IE
Deep vein thrombosis/pulmonary embolism
Bacterial pneumonia superimposed on COVID-19 pneumonia
Influenza A, influenza B
Respiratory syncytial virus
Osteomyelitis
Abscess formation (eg, spinal abscess)
Renal and splenic embolic infarcts
Hepatitis B, hepatitis C
HIV
Tuberculosis

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Author

John L Brusch, MD, FACP Corresponding Faculty Member, Harvard Medical School

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael 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

Michael 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

Disclosure: Nothing to disclose.

Additional Contributors

Barry E Brenner, MD, PhD, FACEP Program Director, Emergency Medicine, Einstein Medical Center Montgomery

Barry 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, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jon Mark Hirshon, MD, MPH, PhD, FACEP Professor, Department of Emergency Medicine, Professor, Department of Epidemiology and Public Health, University of Maryland School of Medicine; Chief, Emergency Department, Baltimore VA Medical Center

Jon Mark Hirshon, MD, MPH, PhD, FACEP 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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Keith A Marill, MD, MS Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Associate Professor, Harvard Medical School

Keith A Marill, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: InCarda Therapeutics<br/>Received ownership interest from General Electric and Medtronic for none. for: Equity ownership: GE Healthcare; Medtronic; Gilead; Cytodyn; Amgen; Pfizer.

Steven 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

Steven 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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.