Case Presentation: Objectives 1. Recognize delayed post infectious vasculitis as a rare complication of bacterial meningitis
2. Recognize the use of corticosteroids for treatment of post infectious vasculitis
Case Description
A 63-year-old man with a one-week history of cough presented with somnolence and a temperature of 102.1°F. The neurological examination showed disorientation and a stiff neck. A cranial CT showed mild ventricular dilation and a sub-acute clotted left ventricular hemorrhage. The CSF yielded 29 cells/uL leukocytes, 1mg/dL glucose and the cultures grew Streptococcus pneumoniae sensitive to penicillin. Treatment was initiated with ceftriaxone and dexamethasone. Over the next week he improved and was back to his baseline. The dexamethasone was discontinued on day 8. On day 10, he again became disoriented and lethargic with fevers to 103 °F. CT head was unchanged. Repeat lumbar puncture yielded 1200 cells/uL leukocytes with neutrophilic predominance and negative cultures. The remainder of infectious work-up was negative – including blood and urine cultures. A MRI brain was obtained and revealed multiple areas of embolic cerebral infarcts; the TEE was unremarkable. The dexamethasone was reinitiated, and his fevers and mental status improved. On day 18, the dexamethasone was switched to prednisone and a taper was initiated. On day 22, he developed disorientation and somnolence again, a repeat MRI brain showed new ischemic infarcts. MRI Angiography of the brain revealed a beaded appearance of the bilateral cerebral circulation. Dexamethasone was reinitiated with improvement in level of consciousness although some neurological deficits persisted. He was discharged to a nursing home with a prolonged dexamethasone taper for post-infectious cerebral vasculitis.
Discussion: Vasculopathy resulting in neurological deficits is a known complication of bacterial meningitis but typically occurs early during the initial stages of infection. Delayed vascular complications are rare. Post infectious cerebral vasculitis typically presents with new neurological deficits despite initial improvement and bacterial clearance. The reappearance of symptoms after discontinuing immunosuppressive treatment suggests that it is likely a post-infectious immune mediated complication. Pathogenesis is not well understood, although a review of limited case reports suggests that Streptococcus pneumoniae can alter host immune response in certain hosts who are susceptible to autoimmune disease. The mainstay of treatment for post-infectious cerebral vasculitis is immunosuppressive therapy: corticosteroids, cyclophosphamide and Intravenous Immunoglobulin (IVIG). Unfortunately despite treatment, morbidity and mortality from progressive neurological insults remains high.
Conclusions: Diagnosing post-infectious vasculitis can be challenging due a lack of specific symptoms but suspicion should be raised in patients with recent bacterial meningitis who present with new recurrent neurological symptoms despite initial improvement and bacterial clearance. Corticosteroids should be initiated promptly if such complications develop and there is no evidence for ongoing infectious processes