Walsh & Hoyt: Vasculitis

Intracranial arteries and veins may become infected by a variety of organisms. The infection may be a primary process within the vascular system itself or may result from the effects of an acute, subacute, or chronic contiguous process that penetrates the vessel. The inflammatory response varies greatly depending on the blood vessels affected, the type of organism responsible, the mode of spread, and the stage of the infectious disease. The principal types of reactions are: (a) the suppurative inflammation produced mainly by pyogenic bacteria; (b) the nonsuppurative or proliferative response seen in typhoid fever and scarlet fever; (c) the hemorrhagic response seen in anthrax, glanders, and some viral infections; and (d) the histiocytic and granulomatous response seen in syphilis, leprosy, and tuberculosis. The sequelae of infectious angiitis also are variable. There may be little or no structural damage. Extensive fibrosis with calcification and luminal stenosis may occur. The vessel may become thrombosed but later recanalize. The vessel may rupture, producing subarachnoid or intracerebral hemorrhage. Finally, the vessel wall may weaken and dilate, resulting in formation of a mycotic aneurysm or pseudoaneurysm. Clinically important infectious angiitis in humans may be caused by a number of different organisms, including pyogenic bacteria, viruses, spirochetes, fungi, and rickettsiae.