Ultrastructural changes in the blood-brain barrier of mice infected with Plasmodium berghei.

Mice infected with the rodent malaria parasite Plasmodium berghei exhibit ultrastructural changes of the blood-brain barrier during the course of infection. Firm adherence including cellular interdigitation of infected cells or leucocytes and even clusters of cells to the vascular-endothelial lining is repeatedly observed early during infection. Ghosts and membrane remnants can be found engulfed in the surface of the endothelial cells. Frequently leucocytes migrate between endothelial cells and even cause a lift off and degeneration of these cells. In addition, endothelial cells exhibit increased pinocytotic activity, many irregular cytoplasmic extensions and even phagocytic activity. These changes are associated with degenerative changes in the basement membrane. Swelling and deposition of collagen-like fibres and even loss of fragments of basement membrane is observed. In some places fingerlike extensions of pericytes passed through the basement membrane and contacted or even bulged into the cytoplasm of endothelial cells. Ballooning and even coalescence of perivascular astrocytes was observed and contributed to the appearance of a perivascular oedematous space. The observed changes indicate a progressive deterioration of the blood-brain barrier eventually leading to endothelial lesions and hemorrhage.

A cytochemical study of cerebrovascular lesions in mice infected with Plasmodium berghei.

Mice with a Plasmodium berghei infection exhibit morphological and cytochemical changes in the blood-brain barrier. Changes in activity and localization of alkaline phosphatase and adenosine triphosphatase, enzymes with important functions in the maintenance of the blood-brain barrier, were observed. Changes in activity and localization of those enzymes in and near the endothelial cells of the microvasculature, concomitant with an increase in pinocytotic activity, and formation of irregular cytoplasmic extensions in these cells, as well as loosening of the basal lamina are indicative of a functional deterioration of the blood-brain barrier in the course of infection.