NECROTIZING BACILLUS-CEREUS INFECTION OF THE MENINGES WITHOUT INFLAMMATORY REACTION IN A PATIENT WITH ACUTE MYELOGENOUS LEUKEMIA - A CASE-REPORT

Citation
N. Motoi et al., NECROTIZING BACILLUS-CEREUS INFECTION OF THE MENINGES WITHOUT INFLAMMATORY REACTION IN A PATIENT WITH ACUTE MYELOGENOUS LEUKEMIA - A CASE-REPORT, Acta Neuropathologica, 93(3), 1997, pp. 301-305
Citations number
19
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
Journal title
ISSN journal
00016322
Volume
93
Issue
3
Year of publication
1997
Pages
301 - 305
Database
ISI
SICI code
0001-6322(1997)93:3<301:NBIOTM>2.0.ZU;2-U
Abstract
A 64-year-old man in a severely immunocompromised state due to acute m yelogenous leukemia died, respirator-unaided, about 10 h after the abr upt onset of coma. An earlier blood culture had yielded Bacillus cereu s. The autopsy, performed 2 h after death, demonstrated diffuse subara chnoid hemorrhage without berry aneurysms, and the formalin-fixed brai n was tinged with gray-brownish discoloration. The sections of the bra in presented a whitish tint of the surface layer of all portion of the cerebral cortices, even those in the sulci. Histological examination of the brain revealed leptomeningeal B. cereus dissemination, and wide spread necrosis of the leptomeninges and arachnoid vessels without inf lammatory cell reaction. The grossly recognizable whitish surface laye r of the cerebral cortex showed overt hyperchromatism, and contained n eurons more degenerative than those located in the deeper cortical lay er. The total absence of inflammatory reaction may be explained by a c ombination of the immunocompromised state of the patient and the chara cter of B. cereus infection, which in itself induces little inflammato ry reaction. The prominent lesions were confined to the cerebral surfa ce layer and leptomeningeal tissue including the arachnoid vessels, wh ich were all bathed in the cerebrospinal fluid, suggesting that some n ecrotizing toxins had been secreted into the fluid by the B. cereus. T he necrosis of arachnoid vessels is thought to have in turn caused dif fuse subarachnoid hemorrhage and marked disturbance of the cerebral bl ood flow, resulting in the terminal coma.