Histochemistry of cerebral lesions in mice infected with Plasmodium berghei.

The brains of mice with established symptoms of Plasmodium berghei erebral malaria were investigated histochemically and histologically. The activity of mitochondrial, lysosomal, glyco/glycogenolytic, hydrolytic and oxidizing enzymes as well as enzymes of the Krebs cycle and the pentose cycle was studied during the course of the infection. For comparison cryostate sections were also stained with haematoxylin and eosin, and according to Kluver-Barrera. Changes in enzyme activity, particularly of the vascular endothelium suggest a functional alteration of the blood-brain barrier which precedes the histochemically detectable lesions of the brain parenchyma. Decrease and total loss of enzyme activity in circumscript areas, also of ependymal cells were indicative of an early ischemic lesion. A population of small, non-phagocytozing, granuloma-like cells frequently accumulating in the frontobasal regions and in the subependymal zones were probably immature astrocytes. During early infection, these cells apparently fail to differentiate and turn to necrosis at the end of the second week. The results of this study support the concept of a triggering role of an initial vascular lesion and a functional breakdown of the blood-brain barrier in susceptible areas of the brain, in the pathogenesis of experimental malaria.