This is the case of a 28-year-old Filipino female diagnosed initially with a right frontal pleomorphic xanthoastrocytoma (WHO grade II, IDH-wildtype), who underwent excision and then stereotactic radiosurgery of the residual tumor. She had a recurrence at 9 months from initial diagnosis, for which she was treated with intensity-modulated radiotherapy and temozolomide concurrently and adjuvantly. She had two more recurrences at 1 year and at 2.4 years from diagnosis. Various combinations of temozolomide and the EGFR inhibitor, nimotuzumab, were given for the recurrent tumor. Four months after the last recurrence, the patient was readmitted for progressive generalized body weakness and anorexia developing over 2 months, accompanied by intermittent fever. There was no associated headache, seizures, decrease in sensorium, or new focal neurologic deficit. At this time, she was on temozolomide and nimotuzumab treatment.
Her past medical history includes histiocytosis in infancy and pulmonary tuberculosis during childhood. She has pet cats and is exposed to feline feces when she does gardening in her backyard.
Upon admission to the hospital, she was persistently febrile. Her complete blood count showed leukopenia (WBC count 3,740 cells/muL; absolute lymphocyte count 374 cells/muL) and thrombocytopenia (platelet count 70,000 cells/muL). Temozolomide was discontinued. She later developed a temporoparietal headache and decreased sensorium. She became drowsy and asthenic but weaker on the left extremities (Medical Research Council muscle strength grading of right upper extremity 4/5, right lower extremity 3/5, left upper extremity 2/5, left lower extremity 1/5). There were no cranial nerve deficits, papilledema, or meningeal signs. On the 8th hospital day, a repeat cranial MRI with contrast was done to workup for tumor recurrence. The cranial MRI revealed multiple vari-sized enhancing lesions in both cerebral hemispheres and in the posterior fossa with perilesional edema on FLAIR sequence (Fig. 1). The known right frontal lobe tumor showed a slight decrease in size and mass effect. Due to the symptoms of fever, headache, and decreasing sensorium in the background of long-term temozolomide use and exposure to feline excreta, a central nervous system infection, particularly toxoplasma encephalitis, was considered. However, the multiple focal lesions precluded a lumbar puncture for this patient due to the risk of brain herniation. Serological workup for toxoplasma (VIDAS  TOXO IgM and VIDAS  TOXO IgG, enzyme-linked fluorescence assays by bioMerieux, Inc.) showed elevated IgM and IgG antibody titers (IgM 0.79 IU/mL [test cut-off = 0.55]; IgG >300.0 IU/mL [test cut-off = 4]). A tuberculosis interferon-gamma release assay was also done, which showed indeterminate results. The patient was treated for possible cerebral toxoplasmosis and was started on trimethoprim-sulfamethoxazole 800 mg/160 mg IV every 12 h. Three days from initiation of antimicrobials, there was lysis of the fever and gradual improvement of her sensorium. A repeat cranial MRI on the second week of treatment showed a slight decrease in the number and size of the enhancing lesions as well as the perilesional edema. Two weeks after hospital discharge, a thallium-201 SPECT scan of the brain was performed to distinguish between toxoplasmosis and tumor recurrence. SPECT images did not show increased tracer uptake in any of the lesions, a finding more consistent with cerebral toxoplasmosis (Fig. 2). The patient completed antibiotic therapy with oral trimethoprim-sulfamethoxazole at 800 mg/160 mg daily for 1 year. Serial cranial MRI images showed a further decrease and eventual resolution of the multiple enhancing lesions. The CARE checklist was accomplished for this case report, attached as online supplementary material (for all online suppl. material, see www.karger.com/doi/10.1159/000529830).