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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.
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]

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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