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Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling
Published on: April 7, 2015
Pathologic findings in native infective endocarditis
Jennifer A Collins1, Yang Zhang1, Allen P Burke1
1From the Department of Pathology, University of Maryland Medical Center, Baltimore, United States.
Background:
There are few studies on the histologic findings in native infective endocarditis, especially regarding mimics of autoimmune valvulitis.
Methods:
We prospectively studied 106 surgical specimens from 95 patients with a clinical diagnosis of infective endocarditis on native valves, and compared gross and histologic findings with culture results, underlying valve disease, risk factors and time interval from symptom onset to surgical intervention.
Results:
There were 41 (39%) aortic, 33 (31%) mitral, 9 (9%) tricuspid, 1(.9%) pulmonic and 11 (10%) multiple valve replacements. Underlying valve disease was present in 26 (27%) patients (non-calcified bicuspid aortic valve, 10 (38%) cases; mitral valve prolapse, 5 (19%) cases; calcified trileaflet aortic valve, 5 (19%) cases; calcified bicuspid aortic valve, 2 (8%) cases; post-rheumatic mitral valve disease, 2 (8%) cases; hypertrophic cardiomyopathy-related mitral valve disease, 1 (4%) case, trileaflet aortic insufficiency 1 (4%) case) and associated with streptococcal infection (p = .001). Absence of underlying valve disease was associated with intravenous drug abuse (p = .01) and dialysis dependent renal disease (p = .006). Intravenous drug abuse was associated with staphylococcal infection (p = .03). Vegetations were present in 80 (75%) of cases, and on the nonflow surface of the valve in 65 (81%) of these. Gram-stain positivity and neutrophilic microabscesses were associated with staphylococcal infection (p = .03). Epithelioid macrophages with palisading features mimicking necrobiotic granulomas were seen in 42 (40%) valves and more frequently associated with streptococcal infection (p=.03). As expected, the presence of valve necrosis and acute inflammation decreased with an increase in time with respect to symptomatic onset.
Conclusion:
Histologic findings that mimic autoimmune inflammation are frequent in infective endocarditis and associated with streptococcal infection. Risk factors for infective endocarditis include calcific valve disease.
Insights
Histologic findings mimicking autoimmune inflammation are common in infective endocarditis, particularly with streptococcal infections. Underlying calcific valve disease is a significant risk factor for this condition.
Area of Science:
- Cardiovascular Pathology
- Infectious Diseases
- Histopathology
Background:
- Limited research exists on the histological characteristics of native infective endocarditis.
- A particular focus is needed on distinguishing infective endocarditis from autoimmune valvulitis based on tissue examination.
Purpose of the Study:
- To prospectively analyze the gross and histological features of native valve infective endocarditis.
- To correlate these findings with microbiological results, pre-existing valve conditions, patient risk factors, and disease progression.
Main Methods:
- Surgical specimens from 95 patients with infective endocarditis were examined.
- Histological analysis included evaluation of vegetations, inflammation, and specific cellular patterns.
- Correlations were made with culture data, underlying valve disease, risk factors, and time from symptom onset.
Main Results:
- Underlying valve disease was present in 27% of patients, often associated with streptococcal infection.
- Absence of underlying valve disease was linked to intravenous drug abuse and dialysis dependence.
- Histological features mimicking autoimmune inflammation (epithelioid macrophages) were observed in 40% of cases, frequently with streptococcal infections.
Conclusions:
- Histological findings that resemble autoimmune inflammation are common in infective endocarditis.
- These mimics are particularly associated with streptococcal infections.
- Calcific valve disease is identified as a risk factor for infective endocarditis.
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