Delayed cerebral thrombosis (DCT) is a devastating cerebrovascular complication in patients with excellent initial recovery of pneumococcal meningitis. The aetiology is unknown, but direct bacterial invasion, activation of coagulation or post-infectious immunoglobulin deposition has been suggested.

We studied histopathology of 4 patients with pneumococcal meningitis complicated by DCT. Results were compared with 8 patients who died of pneumococcal meningitis without DCT and 3 non-meningitis control cases. Furthermore, we evaluated vascular immunoglobulin depositions (IgA, IgG and IgM) and the presence of pneumococcal capsules by immunofluorescence.

Patients who died after pneumococcal meningitis showed inflammation in the meninges and blood vessels with extensive infarction and thrombosis. We did not observe gross differences between DCT and non-DCT patients, except that 2 of 4 DCT patients had a basilar artery aneurysm compared to none of the non-DCT patients. We observed high density of IgM and IgG deposition in meningitis cases as compared to controls, but no difference between DCT and non-DCT patients. Immunofluorescence staining of pneumococci demonstrated the presence of bacterial capsules in the meninges of all meningitis patients, even 35 days after the initiation of antibiotic treatment.

The aetiology of DCT complicating pneumococcal meningitis seems to be of multifactorial aetiology and includes vascular inflammation, thromboembolism of large arteries and infectious intracranial aneurysms. Pneumococcal cell wall components can be observed for weeks after pneumococcal meningitis and may be a source of resurging inflammation after the initial immunosuppression by dexamethasone.