Burkitt Lymphoma (Epstein-Barr Virus - HHV-4)

Primary EBV infection or reactivation in B cells initiates oncogenic transformation.

Chromosomal translocation involving MYC gene activation is the critical genetic event.

Co-infection with Plasmodium falciparum malaria in endemic areas facilitates EBV-driven B-cell proliferation.

Latency between EBV infection and lymphoma development can range from months to years.

Rapid tumor growth leads to symptom onset within weeks to a few months after malignant transformation.

In immunocompromised hosts, latency may be shorter due to impaired immune surveillance.

Initial symptoms often mimic common infections, leading to misdiagnosis as bacterial or viral lymphadenitis.

Rapid tumor growth can be mistaken for acute infections or other malignancies delaying biopsy.

Lack of awareness of Burkitt lymphoma in non-endemic areas contributes to delayed diagnosis.

Limited access to advanced diagnostic tools such as immunophenotyping and cytogenetics can postpone confirmation.

Rapidly growing painless mass in jaw, abdomen, or other extranodal sites.

B symptoms including fever, night sweats, and weight loss.

Abdominal pain or distension due to bowel involvement.

Signs of tumor lysis syndrome such as nausea, vomiting, and confusion.

Neurological symptoms if there is CNS involvement.

Patients typically present with rapidly enlarging, painless lymphadenopathy or extranodal masses.

Common sites include the jaw (endemic form), abdomen, and ileocecal region (sporadic form).

Symptoms progress quickly over days to weeks, often with B symptoms such as fever, night sweats, and weight loss.

Abdominal involvement may cause pain, distension, or bowel obstruction.

Central nervous system involvement can present with neurologic deficits in advanced cases.

History of chronic EBV infection or infectious mononucleosis may be present.

Immunodeficiency conditions such as HIV/AIDS or post-transplant immunosuppression increase risk.

Previous episodes of malaria in endemic regions are relevant.

No specific prior malignancies are typically associated but immunosuppression is a key modifier.

No strong familial inheritance pattern is established for Burkitt lymphoma.

Rare familial cases may be linked to inherited immune deficiencies affecting EBV control.

Family history of other lymphoproliferative disorders may be noted but is not common.

Presence of a rapidly enlarging, painless mass in the jaw or facial bones in endemic Burkitt lymphoma.

Abdominal distension or palpable mass due to involvement of the ileocecal region in sporadic Burkitt lymphoma.

Lymphadenopathy in cervical, axillary, or inguinal regions.

Hepatosplenomegaly may be present due to systemic involvement.

Signs of tumor lysis syndrome such as dehydration or altered mental status in advanced cases.

Aggressive intravenous hydration and allopurinol to prevent tumor lysis syndrome during chemotherapy initiation.

Supportive care including transfusions and infection prophylaxis to manage complications of immunosuppression.

Central nervous system prophylaxis with intrathecal chemotherapy to prevent CNS involvement.