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Published on: September 7, 2022
Splenic infarction in a child with primary Epstein-Barr virus infection
1Department of Pediatrics, School of Medicine, Chungnam National University, Daejeon, Korea.
Insights
A healthy child developed splenic infarction after Epstein-Barr virus (EBV) infection. Transient deficiencies in protein C and S may cause hypercoagulability, leading to this splenic complication.
Area of Science:
- Pediatric Medicine
- Infectious Diseases
- Hematology
Background:
- Epstein-Barr virus (EBV) infection, commonly known as infectious mononucleosis, can present with various complications.
- Splenic infarction is a rare but serious complication, particularly in pediatric cases.
Observation:
- A previously healthy 7-year-old girl presented with abdominal pain and was diagnosed with primary EBV infection.
- She exhibited abnormal liver function and mild splenomegaly.
- Coagulation tests revealed transiently low plasma activity of protein C (49%) and protein S (47%).
Findings:
- The patient developed splenic infarction shortly after the onset of EBV infection.
- The low levels of protein C and S normalized within three weeks.
- This suggests a potential link between EBV infection and temporary deficiencies in these coagulation factors.
Implications:
- Transient deficiencies in protein C and S may lead to a hypercoagulable state.
- This hypercoagulability could be a contributing factor in the development of splenic infarction during infectious mononucleosis.
- Highlights the importance of considering coagulation abnormalities in pediatric patients with EBV and abdominal symptoms.
Abstract:
Described herein is the case of a previously healthy 7-year-old girl who had splenic infarction. This lesion was identified 1 day after the first presentation of peri-umbilical and right upper quadrant pain. She had abnormal hepatic function and mild splenomegaly, and was diagnosed as having primary Epstein-Barr virus (EBV) infection. Coagulation profiles indicated low plasma activity of protein C (49%) and protein S (47%), which normalized 3 weeks later. Hypercoagulability in transient protein C and protein S deficiency might contribute to the development of splenic infarction in infectious mononucleosis.
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