Histology of the brain stem indicates meningitis, edema and hemorrhages that might explain death from suffocation due to direct damage to the respiratory center. Erythrocytes were present within the meningeal space but no clear vasculitis could be detected. We find massive bacterial growth in the meninges without evidence of encephalitis, even when the bacteria emerge from a parenchymal blood vessel. The major histopathological finding is meningitis. anthracis bacteria have a low tendency to adhere to endothelial cells, might suggest that these clots are used as an adherence mechanism by the bacteria.

The high concentration of these aggregates in areas of significant tissue destruction combined with the fact that capsular B. The choroid plexus also contained significant amounts of intravascular bacterial aggregates, often enclosed in what appear to be fibrin-like clots. We found massive destruction of entire sections of the choroid plexus coupled with massive aggregation of bacilli in the ventricles, in close proximity to the parenchyma. Though we could find sporadic growth of the bacteria around blood vessels in the cortex, we report that the main infiltration route is the choroid plexus.

anthracis infection of the central nervous system (CNS). In this manuscript we describe a histopathological study of the B. A similar pathology was observed in animals that succumbed following infection with the toxin deficient mutant, thus indicating that anthrax meningitis is a toxin-independent phenomenon. anthracis-infected animals presented histopathology of meningitis at the time of death, some without any sign of hemorrhage. Recently we demonstrated in Guinea pigs and rabbits that 100% of the B. Hemorrhagic meningitis is considered a complication of anthrax and was reported in about 50% of deadly cases in humans and non-human primates (NHP).

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