Cerebral Toxoplasmosis Masquerading Cns Lymphoma on FDG PET-CT in Post Renal Transplant Patient.

20 year old post renal transplant patient developed recurrent episodes of seizure. MRI revealed focal lesion in right parieto-occipital lobe with perilesional edema. FDG PET-CT revealed multiple hypermetabolic lesions in bilateral cerebral hemisphere. Subsequent biopsy from the lesion demonstrated bradyzoites of Toxoplasma gondii with inflammatory cells and thereby, a confirmatory diagnosis of cerebral toxoplasmosis was made. This case demonstrates the fact that increased FDG uptake in cerebral lesions in post transplant patient should be interpreted with caution and confirmed with histopathological correlation.

A 20 year old post renal transplant patient, who was subsequently kept on immunosuppressive therapy, experienced a single episode of seizure after two years of renal transplant. MRI was advised which revealed a focal lesion in the right parieto-occipital lobe (solid arrow) which was hyperintense on both T2 and T1 weighted images with significant perilesional edema [Figure 1]. A differential diagnosis of post transplant lymphoproliferative disorder (PTLD) vs CNS toxoplasmosis was made and patient was referred for 18F- Fluorodeoxyglucose Positron Emission Tomography-Computed Tomography (FDG PET-CT) for further evaluation. 18F-FDG PET-CT revealed multiple hypermetabolic enhancing lesions involving left parietal lobe, left parasagittal location and right parieto-occipital lobe [Figure 2]. Maximum Standardised Uptake Value (SUVmax) of the lesion in left parasagittal location was 12.5. All the lesions demonstrated greater uptake than normal brain parenchyma. So, a possible diagnosis of PTLD was made. However, for further confirmation brain biopsy was performed from the right parieto-occipital lobe lesion which demonstrated bradyzoites of Toxoplasma gondii with inflammatory cells and thereby a confirmatory diagnosis of cerebral toxoplasmosis was made. The patient was given anti-toxoplasma therapy with pyrimethamine, sulfadiazine, and folinic acid in combination. Subsequent MRI revealed significant reduction in size of the lesion and perilesional edema [Figure 3].

Figure 1

MRI revealed a focal lesion in the right parieto-occipital lobe which was hyperintense on both T2 and T1 weighted images with significant perilesional edema

Figure 2

18F-FDG PET-CT revealed multiple hypermetabolic enhancing lesions involving left parietal lobe, left parasagittal location and right parieto-occipital lobe

Figure 3

Post treatment MRI revealed significant reduction in size of the lesion and perilesional edema

Toxoplasma gondii is a protozoan parasite, which causes opportunistic infections in the immunocompromised, as in solid-organ transplant.[12] PTLD is a serious complication of solid organ transplantation with incidence in renal transplant recipients of -1-4%. Central nervous system (CNS) lymphoma is a rare form of PTLD and is more common after renal transplantation.[3] The distinction between primary CNS lymphoma and cerebral toxoplasmosis is important because of difference in the treatment. Cerebral toxoplasmosis can be treated with medication, whereas primary CNS lymphomas are usually treated with radiation therapy and corticosteroids.[4] However, neither CT nor MRI scans can reliably distinguish CNS toxoplasmosis from lymphoma.[5] Several authors reported the usefulness of FDG PET to differentiate cerebral toxoplasmosis from primary CNS lymphoma. Villringer et al.[6] compared FDG uptake within the lesion with the uptake in a contralateral brain area. In all subjects with CNS toxoplasmosis, the FDG uptake ratio was significantly lower than the FDG ratio in patients with lymphoma. Hoffman et al.[7] also reported significant difference between FDG uptake in lymphoma and cerebral toxoplasmosis. Westwood et al.[8] also reported the utility of FDG PET-CT in differentiating CNS toxoplasmosis from PTLD. However, all the above mentioned studies were performed in the settings of HIV infection. Whether similar difference exists in the settings of solid organ transplant is a matter of debate. Furthermore, in contrast to the findings of the above mentioned studies, we have found significant higher uptake in the lesions of CNS toxoplasmosis in a post renal transplant patient. Therefore, increased FDG uptake of the cerebral lesion in patients with solid organ transplant should be interpreted with caution in differentiating CNS toxoplasmosis from PTLD and should be confirmed by histopathological evaluation.

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