The histologic findings in a serially sectioned temporal bone, from a patient who succumbed to brain abscess secondary to necrotizing (“malignant”) external otitis, are described. The mechanism of invasion of the ear canal appears to be due to local bone necrosis. This in turn extends to the submucosal vasculature of the pneumatic spaces. The infective process extends submucosally, establishing one or several sites of bone destruction. The lumen of the pneumatic space is not involved. In this process, the periphery of the fibrous inflammatory tissue formation is the site of active bone destruction. In pneumococcal petrositis, the peripheral fibrous elements are protective. The process in malignant external otitis may extend directly to adjacent central nervous system structures inoculating the structure with Pseudomonas. Development of Pseudomonas brain abscesses can be slow, allowing for new bone closure of the site from which the infection spreads as demonstrated in this specimen. Therefore, apparent local control of the disease can be established while a central infective process progresses.