Infective Endocarditis Differential Diagnoses

  • Author: John L Brusch, MD, FACP; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Nov 29, 2011
 
 

Diagnostic Considerations

Definitive diagnosis of infective endocarditis (IE) is generally made by using the Duke criteria.

Duke diagnostic criteria

Durack and colleagues developed diagnostic criteria that combine the clinical, microbiological, pathological, and echocardiographic characteristics of a specific case.[48]

Major blood culture criteria include the following:

  • Two blood cultures positive for organisms typically found in patients with IE (ie, S viridans, Streptococcus bovis, a HACEK group organism, community-acquired S aureus, or enterococci in the absence of a primary focus)
  • Blood cultures persistently positive for one of the above organisms from cultures drawn more than 12 hours apart
  • Three or more separate blood cultures drawn at least 1 hour apart

Major echocardiographic criteria include the following:

  • Echocardiogram positive for IE, documented by an oscillating intracardiac mass on a valve or on supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation
  • Myocardial abscess
  • Development of partial dehiscence of a prosthetic valve
  • New-onset valvular regurgitation

Minor criteria include the following:

  • Predisposing heart condition or intravenous drug use
  • Fever of 38°C (100.4°F) or higher
  • Vascular phenomenon, including major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions
  • Immunological phenomenon such as glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor
  • Positive blood culture results not meeting major criteria or serologic evidence of active infection with an organism consistent with IE (eg, Brucella, C burnetii [ie, Q fever], Legionella)
  • Echocardiogram results consistent with IE but not meeting major echocardiographic criteria

Definitive pathological diagnosis is established by demonstrating microorganisms, by culture or histology, in vegetations removed by surgery, embolectomy, or drainage of an intracardiac abscess. Alternatively, a definitive clinical diagnosis is made based on the presence of 2 major criteria, 1 major criterion and 3 minor criteria, or by 5 minor criteria.

A diagnosis of possible IE is made when findings consistent with IE fall short of the criteria for definite IE but do not meet the criteria for rejection.

Rejection criteria for the diagnosis of IE are as follows:

  • The presence of a firm alternative diagnosis of the manifestations of endocarditis
  • Resolution of manifestations of endocarditis after 4 or fewer days of antimicrobial therapy
  • No pathologic evidence of IE at surgery or autopsy after 4 or fewer days of antimicrobial therapy

These criteria may, at times, overdiagnose IE and may not be as applicable in patients with subacute disease.

Other problems to be considered include the following:

  • Thrombotic nonbacterial endocarditis
  • Vasculitis
  • Temporal arteritis
  • Marantic endocarditis
  • Connective tissue disease
  • Fever of unknown origin (FUO)
  • Intra-abdominal infections
  • Septic pulmonary infarction
  • Tricuspid regurgitation

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
Author

John L Brusch, MD, FACP  Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

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

Disclosure: Nothing to disclose.

Coauthor(s)

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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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

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

Disclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. Ownership interest None; General Electric Ownership interest None

Specialty Editor Board

Jon Mark Hirshon, MD, MPH  Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine

Jon 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

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Thomas M Kerkering, MD  Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas 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

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

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, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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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 Administration 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 Administration 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.
A young adult with a history of intravenous drug use diagnosed with right-sided staphylococcal endocarditis and multiple embolic pyogenic abscesses on chest radiograph.
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 the cases are not associated with underlying valvular disease.
  • The mortality rate of S aureus IE is 40-50%.
  • S 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 acquired not only in the hospital but also in any type of health care 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.
  • S intermedius infection accounts for 15% of streptococcal IE cases.
  • S intermedius is unique among the streptococci; it can actively invade tissue and can cause abscesses.
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.[17]
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.
  • IE 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.[18]
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