Abstract Introduction Toxoplasmosis infections in immunocompetent individuals classically presents as a subclinical or self-limiting disease. Immunosuppressed patients are at risk for reactivation which can manifest as central nervous system (CNS) involvement1. CNS toxoplasmosis is the leading cause of intracerebral masses in acquired immunodeficiency syndrome, solid organ transplant recipients, and patients receiving cytotoxic chemotherapy 2. CNS toxoplasmosis is exceedingly rare in patients without human immunodeficiency virus or solid organ transplantation 3. We present a case of delayed identification of cerebral toxoplasmosis in a systemic lupus erythematosus (SLE) patient on mycophenolate mofetil (MMF). Case Presentation A 72 year old female with type 2 diabetes mellitus and SLE on MMF was brought to an outside hospital for acute altered mental status and seizures. She was found unresponsive with a witnessed seizure with left gaze deviation. Imaging revealed an acute ischemic infarct with a newly reduced ejection fraction, but was not a candidate for thrombolytic therapy. She was transferred to our hospital for an ischemic evaluation, but cardiac catheterization was deferred given her mental status. Video electroencephalography (EEG) showed no evidence of seizure. Brain MRI showed numerous foci of reduced diffusion and enhancement most pronounced in the left temporal occipital lobe concerning for septic emboli or infection (Figure 1). Initial lumbar puncture (LP) was lymphocytic-predominant with elevated protein with a negative infectious/autoimmune evaluation. She was continued on empiric intravenous ceftriaxone and vancomycin given concern for culture negative endocarditis. On hospital day 25, she aspirated and required intubation. Given progression of brain imaging suspicious for toxoplasmosis, she was started on empiric trimethoprim/sulfamethoxazole and underwent repeat LP with a positive toxoplasma PCR. Toxoplasma serum studies returned positive for IgG with negative IgM. She experienced a mild improvement in her mental status but required tracheostomy and ultimate discharge to an acute rehab facility on hospital day 73. Discussion Early recognition of CNS toxoplasmosis is critical as the majority of patients will experience neurologic improvement with prompt treatment 4. Delayed treatment can result in seizures, coma, and/or significant mortality; thus, empiric therapy should be started prior to obtaining confirmation 5. Cerebral toxoplasmosis in a patient on MMF monotherapy is exceptionally rare with only 2 cases currently existing in the literature 6. Conclusion We argue that MMF may increase the risk of toxoplasmosis reactivation predisposing patients to CNS toxoplasmosis. Given the substantial associated morbidity, clinicians should have a higher index of suspicion for CNS toxoplasmosis in patients immunosuppressed with MMF. Figure 1: This abstract is funded by: None
Sayegh et al. (Fri,) studied this question.