A54-14 Ring Enhancing Lesion of the Spinal Column in the Setting of New Onset Cerebral Toxoplasmosis

Abstract Introduction Toxoplasma gondii is an opportunistic parasitic infection seen primarily in immunocompromised hosts (e.g., HIV with CD4 200/µL, malignancy, or transplant) (1,2,3). Transmitted via undercooked meat or oocysts from cats, the parasite invades intestinal and immune cells, crossing the blood-brain barrier to cause Central Nervous System (CNS) disease (1,3). Symptoms include headache, weakness, altered mental status, seizures, and focal deficits (1,2). Diagnosis involves serology (IgG/IgM), PCR of cerebral spinal fluid (CSF), and neuroimaging (CT scan and MRI) showing ring-enhancing lesions often mimicking CNS lymphoma (1,2). Standard therapy includes pyrimethamine with sulfadiazine or clindamycin. While CNS invasion is well documented, spinal involvement is exceedingly rare (4); this case may represent the first with both cerebral and spinal toxoplasmosis. Case A 51-year-old woman with hypertension presented with altered mental status, weakness, and lethargy. Imaging revealed multiple ring enhancing lesions with a large right frontal mass and vasogenic edema. Initial concern was for malignancy, but biopsy showed necrosis and inflammation. CSF analysis confirmed Toxoplasma gondii, subsequently the patient was newly diagnosed with HIV-1 infection and acute-on-chronic toxoplasmosis reactivation was suspected. MRI of the cervical spine also revealed a C6 lesion concerning for possible spinal involvement. The patient was treated with Pyrimethamine, Sulfadiazine, Leucovorin, and started on antiretroviral therapy (Dolutegravir + Truvada) with Mycobacterium Avium Complex (MAC) and Pneumocystis jirovecii Pneumonia (PJP) prophylaxis. She experienced breakthrough seizures managed with Levetiracetam, Lacosamide, and Benzodiazepines. Serial MRIs showed improvement in cerebral lesions and stability of spinal findings, supporting a diagnosis of cerebral and possible spinal toxoplasmosis with partial response to therapy. Discussion Schlüter et al. demonstrated the mechanism by which Toxoplasma gondii invades the CNS, suggesting spinal involvement is theoretically possible (3). However, reports of spinal calcified lesions linked toxoplasmosis are exceedingly rare, with prior studies unable to confirm causation (4). In this case, a patient with sero-positive cerebral toxoplasmosis, had imaging findings consistent with cerebral toxoplamosis and also subsequently had improvement in both cerebral and spinal calcified lesions treated with Pyrimethamine and Sulfadiazine. This strongly supports toxoplasmosis as the cause, likely representing a false-negative biopsy, consistent with known limitations in diagnostic sensitivity. Conclusion In conclusion, the authenticity of this case having confirmed sero-positive toxoplasmosis, having intracranial calcified lesions that rule out malignancy on biopsy, and observing improvement in the calcified lesions after treatment of toxoplasmosis provides strong evidence to suggest that toxoplasmosis can cause both cerebral and spinal calcifications. This abstract is funded by: None