Spleen, Infectious Mononucleosis, EBER stain

Spleen, Infectious Mononucleosis, H&E stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows H&E stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, H&E stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows H&E stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, CD20 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows CD20 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, CD3 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows CD3 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, CD4 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows CD4 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, CD8 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows CD8 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, Granzyme stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows Granzyme stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, CD30 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows CD30 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, CD138 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows CD138 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, Kappa stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows Kappa stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, Lambda stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows Lambda stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, MIB-1 stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows MIB-1 stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis
Spleen, Infectious Mononucleosis, EBER stain
Details
Disease Category
Gender
Clinical History

25 year-old male with splenic rupture.

Molecular studies on the splenic tissue: negative for B-cell clonality, positive for T-cell clonality.

Case Discussion

Infectious mononucleosis is a benign self-limited lymphoproliferative disorder caused by infection with Epstein-Barr virus (EBV). Symptoms typically include fever, sore throat, lymphadenopathy, splenomegaly, and characteristic atypical lymphocytes in the peripheral blood.

The splenic architecture is preserved but slightly distorted. There is an increase of tingible body macrophages, immunoblasts and plasma cells. Evidence of capsular rupture is also seen. Some immunoblasts may resemble Hodgkin-Reed-Sternberg cells.

Most of the lymphocytes are CD3/CD8+ cytotoxic T-lymphocytes. While the T-cell clonality is positive, the T-cells are reactive. They are not atypical and sometimes, small T-cell clones may be seen in reactive conditions (molecular finding will reveal if oligoclones are present or if a major dominant clone is present, as the latter does not support a benign process). Immunoblasts may be CD30+. EBV is positive in many cells.

The differential diagnosis includes:

Peripheral T-cell lymphoma – but there is no atypia in the T-cells.
Classical Hodgkin lymphoma – but the immunoblasts in this biopsy are not consistent with Hodgkin cells.

The clinical history of splenic rupture also fits with the splenomegaly that can result from infectious mononucleosis. Note that the diagnosis is made after making all considerations. The clinical history is important but should not form the sole basis for the diagnosis.

While the findings are abnormal, the preservation of architecture suggests a benign process.

This slide shows EBER stain. See related content for other stains.

Diagnosis
Infectious Mononucleosis