MR Imaging in toxoplasmosis encephalitis after bone marrow transplantation: paucity of enhancement despite fulminant disease
Summary: We present a patient who underwent bone marrow transplantation (BMT) after developing chronic myelocytic leukemia. Four months after BMT, he became comatose and died. MR imaging revealed multifocal brain lesions that were progressive but produced no edema. Postcontrast studies revealed that most of the lesions were nonenhancing. There was only discrete, irregular leptomeningeal enhancement with possible minimal enhancement of the cortex and subcortical white matter. Autopsy showed overwhelming toxoplasmosis encephalitis. This case illustrates that toxoplasmosis lesions may lack obvious contrast enhancement in the brain of the immunocompromised patients, despite severe involvement. Recognition of this unusual MR imaging manifestation of toxoplasmosis should lead to earlier diagnosis and treatment.
Toxoplasmosis encephalitis is an opportunistic infection most commonly seen in AIDS patients. At MR imaging, lesions are multiple, commonly located in the deep central nuclei, posterior fossa or lobar at the gray-white matter junction, with prominent associated mass effect and edema. After gadolinium administration, the lesions typically show intense parenchymal enhancement (1). After bone marrow transplantation (BMT), brain infections occur with a frequency of 2–4%. The spectrum of infections is variable, favoring bacteria, fungi, or viruses (2). Cerebral toxoplasmosis is a rare complication after BMT, with a prevalence of less than 1% in the United States (3). We report the case of a patient who developed fatal cerebral toxoplasmosis characterized by multiple progressive MR imaging lesions that showed a surprising paucity of enhancement and lack of edema on serial studies.
American Journal of Neuroradiology
(2004). MR Imaging in toxoplasmosis encephalitis after bone marrow transplantation: paucity of enhancement despite fulminant disease. American Journal of Neuroradiology, 25(2), 270-273.
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