Progressive Multifocal Leukoencephalopathy Presenting as Expressive Aphasia in a Lung Transplant Recipient

IntroductionProgressive multifocal leukoencephalopathy (PML) is a demyelinating brain disease caused by reactivation of JC virus in immunocompromised patients. PML typically manifests with subacute neurologic deficits including altered mental status, motor deficits, limb ataxia, gait and visual symptoms. We report an atypical presentation lung transplant recipient (LTR).Case ReportA 71-year-old LTR received rituximab induction followed combination mycophenolate mofetil, tacrolimus, prednisone. He had single episode minimal acute cellular rejection early after LT, but never required significantly augmented immunosuppression. Notably, he mild leukopenia throughout his post-LT course (WBC count 3-4 thousand/µL), no response to 4 doses the Pfizer SARS-CoV-2 vaccine, suggesting advanced At 14 months patient reported progressive anomia aphasia, other deficits. MRI showed abnormal increased T2/FLAIR signal left posterior parieto-occipital subcortical white matter, involving U fibers, characteristic (Figure A, C). Serum PCR low-level viremia, CSF from 2 lumbar punctures was negative. Thus, diagnosed possible PML, immunosuppression narrowed tacrolimus (goal trough 4-6) prednisone, 5 mg daily. Despite reduced immunosuppression, repeat initial diagnosis worsening B, D) symptoms progressed severe anomia, cortical blindness, still deficits.SummaryPML rare, albeit well described, complication only aphasia unusual. Without viral isolation, definitive requires tissue; however, changes fibers area are highly characteristic. Early recognition allows for expeditious management. Progressive (LTR). A