Early cerebral vasculitic infarcts in acute pneumococcal meningitis

A 20-year-old man without any premorbid illness was brought to the emergency department with the history of high-grade fever and headache since two days. He developed two episodes of generalized tonic clonic seizures and lapsed into altered sensorium. On examination, he was febrile and stuporous with Glasgow coma scale (GCS) score of 10, and had neck stiffness with normal fundus examination. The possibility of meningoencephalitis was considered. He was intubated, and required mechanical ventilatory support. Haemogram revealed total leucocyte count of 39,500 per microliter with neutrophilic predominance. Other routine laboratory parameters including serology were unremarkable. Electrocardiography (ECG), chest X-ray, and abdomen ultrasound did not reveal any significant abnormality. Computed tomography of brain was normal. Cerebrospinal fluid (CSF) analysis revealed a total count of 1750 cells/cumm with 90% neutrophils, protein of 164 mg/dl, sugar of 24 mg/dl, and adenosine deaminase (ADA) of 2 u/l; Gram staining showed gram-positive cocci in pairs. Pending the culture reports, he was started on meningitis doses of intravenous ceftriaxone and vancomycin in addition to intravenous levetiracetam and supportive care. By next twentyfour hours, sensorium improved significantly, and was extubated. He was noted to have mild weakness of right upper and lower limbs. Magnetic resonance imaging (MRI) of brain with intravenous gadolinium contrast showed leptomeningeal enhancement in bilateral cortical sulci and in basal cisterns (Figure 1, A) and multiple foci of restricted diffusion in subcortical and deep white matter in bilateral cerebral hemispheres more on left side (Figure 1, B). MRA was unremarkable with no evidence of arterial stenosis or occlusion of intracranial arteries (Figure 1, C). CSF culture confirmed pneumococcal growth sensitive to both ceftriaxone and vancomycin. Work up for alternative causes of stroke in young including vasculitic markers, prothrombotic profile, and trans-esophageal echocardiogram was non-contributory.