Persisting Vasculitis After Pneumococcal Meningitis

Abstract

Parainfectious vasculitis may respond to late corticosteroid treatment. MMP-9 level in CSF may be a marker of vasculitic complication in bacterial meningitis.

Prevention of Brain Injury by the Nonbacteriolytic Antibiotic Daptomycin in Experimental Pneumococcal Meningitis

“…TIMP-1 primarily complexes with MMP-9 and thus inhibits the biological effect of excess MMP-9. In a patient with pneumococcal meningitis, increasing levels of MMP-9 in CSF were associated with persisting vasculitis and delayed brain injury beyond 4 days after the initiation of antibiotic therapy (44). MMP-9 has been identified as an important contributor to brain damage in patients with bacterial meningitis (25).…”

“…In situ zymography experiments detected increased gelatinolytic activity within the meninges, the subarachnoid space, the penetrating vessels, and the perivascular space. An excess of MMP-9 has been found to contribute to the development of cortical lesions in patients with bacterial meningitis and in experimental models (44,47). In children with bacterial meningitis, high levels of MMP-9 were identified as a risk factor for persisting neurological sequelae (27).…”

Infectious Vasculopathy of Intracranial Large- and Medium-Sized Vessels in Neurological Intensive Care Unit: A Clinico-Radiological Study

“…Infection is a well-recognized cause of CNS vasculopathy [5,6]. So far, viruses such as varicella zoster virus (VZV) [7], bacteria including mycobacteria and spirochetes [8][9][10][11][12], fungi, and parasites [13] have been identified as causative agents of cerebral vasculitis. In this study, we retrospectively assessed all patients treated in the neurological intensive care unit of our institution with the diagnosis of nonatherosclerotic intracranial vasculopathy over a period of 10 years.…”

Invasive pneumococcal disease complicated by cerebral vasculitis, transient diabetes insipidus and spondylodiscitis

“…Case death rates and risk of sequelae following meningitis are reported to be higher for S pneumoniae than Neisseria meningitidis or Haemophilus influenzae 5 6 7 12. Even if correct antimicrobial therapy is initially chosen, the proinflammatory cascade triggered by S pneumoniae and self-perpetuated by a dysregulated host inflammatory response will trigger mediators with vascular toxicity resulting in vasculitis syndromes 2 4 7 13. CNS vasculitis involvement has been reported to include seizures (27.6%), diffuse brain swelling (28.7%), hydrocephalus (16.1%), hearing loss (19.5%) and ischaemic or haemorrhagical brain damage (21.8%), being 67% of the ischaemic injuries caused by identified arteritis 2 7…”

“…Pneumococcal meningitis remains a potentially devastating disease with high mortality rate and neurological damage among those who survive 1 2 7 8. Focal neurological findings may be present during the acute phase of bacterial meningitis, but more often occur after a few days as immunological complication of meningitis.…”