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Lymphocytic Myocarditis in Children with Parvovirus B19 Infection: Pathological and Molecular Insights
Lisann Pelzl1, Sabrina Mantino1, Martina Sauter1
1Cardiopathology, Institute for Pathology and Neuropathology, University Hospital of Tuebingen, 72076 Tuebingen, Germany.
Insights
Parvovirus B19 (B19V) causes severe lymphocytic myocarditis in young children. Early diagnosis via endomyocardial biopsies is crucial for treatment and preventing severe outcomes.
Area of Science:
- Pediatric Cardiology
- Viral Pathogenesis
- Immunohistochemistry
Background:
- Investigating the role of parvovirus B19 (B19V) in pediatric myocarditis.
- Utilizing post-mortem samples from affected children.
Purpose of the Study:
- To evaluate B19V's role in pediatric myocarditis pathogenesis.
- To assess diagnostic strategies for viral myocarditis.
Main Methods:
- Analysis of 306 acute and 1060 chronic lymphocytic myocarditis cases (2004-2023).
- Utilized endomyocardial biopsies (EMBs) with histology, immunohistochemistry, and molecular pathology.
- In situ hybridization and molecular detection of B19V DNA/mRNA.
Main Results:
- B19V infection found in 43% of acute vs. 14% of chronic myocarditis cases.
- Higher viral loads in acute myocarditis, particularly in children < 2 years.
- B19V replicated in endothelial cells and B lymphocytes; severe cases noted in infants.
Conclusions:
- B19V is a significant cause of severe lymphocytic myocarditis in young children.
- Combined histopathological and molecular analysis of EMBs aids early viral myocarditis diagnosis.
- Prompt diagnosis and therapy are essential for preventing severe disease.
Background:
This study aims to evaluate the role of parvovirus B19 (B19V) in the pathogenesis of myocarditis in a paediatric population, including post-mortem samples from two children.
Methods:
From 2004 to 2023, endomyocardial biopsies (EMBs) from children under 16 years of age were analyzed using histology, immunohistochemistry, and molecular pathology. A total of 306 children with acute and 1060 children with chronic lymphocytic myocarditis were identified.
Results:
B19V infection was more frequent in acute myocarditis than in chronic myocarditis (43% vs. 14%), with higher viral loads in acute cases regardless of age. The most prominent cardiac CD3+ T cell infiltration was noted in children < 2 years, correlating with high cardiac B19V loads. In two male infants who died from B19V infection, B19V DNA was localized in the endothelial cells of multiple organs using in situ hybridization. Virus replication was found in the endothelial cells of small cardiac arterioles and venules but not in capillaries. B19V DNA/mRNA was also detected in immune cells, especially in the spleen and lymph nodes, revealing virus replication in B lymphocytes.
Conclusions:
B19V can induce severe lymphocytic myocarditis, especially in young children. The simultaneous histopathological and molecular assessment of EMBs is important for early diagnosis of viral myocarditis, preventing severe disease, and ensuring appropriate therapy.
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