A 27-year-old man presented to our hospital with a three day history of headaches and altered mental status. He was having seizures on arrival. He had a Glasgow Coma Scale (GCS) of 4 upon arrival. His pupils were anisocoric and sluggish to light. His brainstem reflexes were intact. Motor exam revealed extensor posturing in bilateral upper extremities and triple flexion in bilateral lower extremities in response to noxious stimuli. He received lorazepam in the emergency room with minimal improvement and was ultimately intubated for airway protection. Computed tomography (CT) head showed regions of hypoattenuation involving bilateral basal ganglia and thalami with superimposed acute hemorrhage, significant mass effect, and patchy regions of acute hemorrhage in the cerebellum. Magnetic resonance imaging (MRI) brain revealed areas of confluent FLAIR signal abnormality in the deep white matter, bilateral basal ganglia and thalami, brainstem, and throughout the cerebellum. He had a hypercellular cerebral spinal fluid (CSF) analysis that showed white blood cell count of 218 with lymphocytic predominance. Protein was elevated to 412 mg/dl and glucose was 17 mg/dl. He was found to be HIV-1 positive with a CD4 count of 6 cells per cubic centimeter. CSF specific toxoplasmosis PCR showed 730,000 copies/milliliter. He was treated with solumedrol and broad-spectrum antimicrobials with minimal improvement in his clinical picture and ultimately succumbed to his disease.