Poster Abstracts

3034 Streptococcus pneumoniae meningoencephalitis with multiple white matter infarcts likely secondary to vasculitis

Abstract

Background Streptococcus pneumoniae meningoencephalitis is associated with high mortality and morbidity. Cerebral vascular occlusion is a known complication, thought to be secondary to direct a-hemolytic invasion and/or post-infectious immune-mediated vasculitis. We report a rare case of extensive subacute infarcts likely secondary to vasculitis associated with streptococcal meningoencephalitis.

Results A 56-year-old woman with reduced consciousness was intubated and transferred to our hospital. She had raised inflammatory markers (C-reactive protein 286) but remained afebrile. Cerebrospinal fluid isolated Streptococcus pneumoniae (DNA/culture positive, protein 12343mg/L, glucose <0.1mmol/L, leukocytes 46X106/L, polymorph 44X106/L, monocyte 2X106/L, erythrocytes 22X106/L) despite negative serial blood cultures. CT non-contrast revealed diffuse left paranasal sinus mucosal thickening and bilateral mastoid air cell effusions with extension into the right middle ear cavity. Right middle ear fluid obtained 2 days after antibiotic initiation was purulent although culture negative. MRI brain on day 3 revealed an unusual pattern of extensive, multifocal bilateral acute infarcts in the supratentorial white matter in a perivascular distribution with no enhancement. MRI on day 11 demonstrated expected evolution of the infarcts and enhancement within mastoid air cells and petrous apices and new leptomeningeal enhancement over bilateral paramedian peri-rolandic cortices, brainstem and the entire spinal cord. She was treated with ceftriaxone, dexamethasone and intravenous immunoglobulin. At 3 months, she followed 1-stage command but remained nonverbal.

Conclusions Multiple white matter infarcts are an unusual complication of pneumococcal meningoencephalitis. The deep white matter is supplied by cortical perforators. This distribution of infarcts is consistent with a vasculitic rather than embolic aetiology.

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