Infectious Disease Online
Pathology of Infectious Mononucleosis (Epstein-Barr Virus Infection)
Syn: Kissing disease
Epstein-Barr virus was discovered during ultrastructural studies of endemic Burkitt’s lymphoma in Africa.
There is now strong evidence that the virus causes two cancers endemic Burkitt’s lymphoma in Africa and nasopharyngeal carcinoma, especially in the Orient.
Epstein-Barr virus is a gamma-group herpes virus that causes a benign, self-limited lymphoproliferative disease that is characterized by fever, generalized lymphadenopathy, splenomegaly, sore throat and appearance in the blood of atypical activated T-lymphocytes.
The virus is spread by intimate oral contact among adolescents (also known as kissing disease). It is usually transmitted through the saliva.
Epstein-Barr virus enters the epithelial cell cytoplasm by directly fusing with the plasma membrane. Epstein-Barr virus enters the B-cell cytoplasm by fusing with the endosomal membranes.
Two EBV proteins, EBNA2 and LMP-1, are associated with B-cell immortalization, which may occur in latently infected lymphocytes.
In infectious mononucleosis, the total white cell count increases to as many as 18,000, 95% of which are atypical T-lymphocytes with an abundant, finely granular, basophilic cytoplasm, containing small fenestrations.
The lymph nodes in the posterior cervical, axillary, and groin regions are enlarged , show increased number of T-cells in their paracortical zones and contain large binucleate cells, Reed-Sternberg-like cells.
With impaired immunity, infectious mononucleosis may become chronic and transform into B-cell lymphoma.
In Burkitt lymphoma associated with EBV there is a characteristic 8:14 translocation, in which the c-myc oncogenes is placed into the immunoglobulin heavy chain expression region.
The pathologic changes are prominent in the lymph nodes and spleen because of the underlying immunologic nature of the illness.
In most patients the lymphadenopathy is symmetrical and most striking in the neck, and the nodes are movable, discrete, and tender.
On gross examination they are soft and swollen and the hyperemic (pink) cut surfaces occasionally display foci of necrosis.
Microscopically, the general architecture is preserved.
The germinal centers are large and have indistinct margins because of proliferation of immunoblasts.
They contain frequent mitoses and scattered nuclear debris, presumably from degenerated B-cells.
The nodes contain occasional large hyperchromatic cells with polylobated nuclei that resemble Reed-Sternberg cells.
The immunoblastic hyperplasia and consequent architectural distortion, and the presence of atypical cells, may present diagnostic problems because of the morphologic similarity to Hodgkin’s disease or non-Hodgkin’s lymphoma.
The spleen is large and soft owing to hyperplasia of the red pulp and is susceptible to rupture.
Many immunoblasts are present throughout the pulp and infiltrate the walls of vessels, the trabeculae, and the capsule.
The edema and infiltration of the capsule probably account for the tendency to rupture.
The liver is almost always involved, but the hepatitis is nonspecific.
The sinusoids contain atypical lymphocytes, and there are mild lymphocytic infiltrates in the portal tracts.
Most patients recover completely, although convalescence may be protracted.
Uncommon neurologic complications include diffuse or focal encephalitis (sometimes involving the cerebellum) and occasionally, aseptic meningitis.
In the rare fatal cases, meningoencephalitis is the most common cause of death.
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