Page 58 - The Vasculitides, Volume 1: General Considerations and Systemic Vasculitis

34 David S. Younger

Bacterial Meningitis

The category of secondary vasculitides related to infection includes acute bacterial and
mycobacterial meningitis, spirochete organisms notably neurosyphilis, LNB, and viral agents
notably VZV, and HIV/AIDS.

The relationship between vascular and parenchymatous cerebral changes including
vasculitis, and acute and chronic neurological symptoms and signs was studied extensively in
9 infants and 5 children by Adam and colleagues [147] with Hemophilus (H.) influenzae
meningitis. Fever, stiff neck, and alteration of consciousness followed a respiratory infection,
with subsequent enlargement of the head and separation of the fontanels, followed later by
lethargy, coma and death despite sulfadiazine antibiotics and antiserum in the earliest stages
of meningitis lasting one to two weeks (7 patients), moderate stages of two to four weeks
(4 patients) or late in the stage of meningitis of more than four weeks (three patients).
Vascular inflammation by neutrophilic cells so noted in five patients (36%) was typified by
inflammation of meningeal veins (2 patients) or meningeal arteries (1 patient) among those
with early stage meningitis involvement; with involvement of meningeal arteries in the
moderate stage patient, and in subarachnoid arteries of the patient in late stage meningitis.
Vascular inflammation was absent in nine patients (63%), four of whom manifested vascular
endothelial hyperplasia of meningeal vessels, while the remaining five were reported to have
no vascular alterations. Based upon the clinicopathological findings, the authors [147]
proposed that from the earliest stages of meningitis, pathological changes could be found in
small and medium sized subarachnoid arteries and veins comprised of neutrophilic cellular
inflammation accompanied by endothelial cell swelling, multiplication and crowding of
lumina, a reaction that ensued over 48 to 72 hours. This was followed by infiltration of
adventitial connection by neutrophilic cells, and in the intima of arteries accompanied by
lymphocytes forming a conspicuous layer. Foci of vascular necrosis occurred in some cases.
Vascular inflammation of the adventitia of subarachnoid vessels was believed to be due to
involvement of the arachnoid membrane which formed the adventitia of the subarachnoid
vessels, thus in a sense, the vessel wall was affected from the very beginning by the
inflammatory process arising within itself. Subintimal inflammation was believed to have an
origin in the foci of necrosis with spread beneath the intima along the line of least resistance.
Spinal and cranial nerves surrounded by purulent exudates from the beginning of the
infectious process at the base of the brain, were infiltrated by inflammatory cells only after
several days, and not very pronounced in comparison to meningeal and cortical vessels, with
comparatively more lymphocytes. Among 34 other infants and children reported by Smith
and Landing [148] with H. influenzae meningitis of 2 to 42 days, six postmortem studied
patients showed involvement of arterial vessels and venous lesions in 10 cases, three of whom
had cortical necrosis and concomitant arteritis, and five had phlebitis. However in only one
patient, a 10-week-old infant who died the evening of admission was arteritis believed to be
responsible for brain damage. In this subject, postmortem examination disclosed acute
inflammation of the walls of several veins and small arteries in the polymorphonuclear
meningeal exudate overlying the cortical surface and extending into the superficial cortex,
with narrowing of the lumina by endothelial proliferation and fibrin thrombi, associated with
extensive early cortical necrosis.

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