IMMUNOPATHOLOGICAL ASPECTS OF PLASMODIUM-BERGHEI INFECTION IN 5 STRAINS OF MICE .2. IMMUNOPATHOLOGY OF CEREBRAL AND OTHER TISSUE LESIONS DURING THE INFECTION

Abstract

Histological changes during the course of P. berghei infection were investigated in A/J, BALB/c, OF1, CBA and C57Bl mice. The findings were studied in relation to serological aspects. High mortality and acute deaths occurred in A/J, BALB/c and OF1 mice and marked cerebral lesions were found in these strains from day 15, including congestion of meningeal and cerebral veins and capillaries, blocking of these vessels by heavily parasitized red blood cells, cerebral edema and hemorrhages. Such lesions were minimal in CBA and C57Bl mice, and absent in mice examined 21 and 24 days after infection. Small IgG deposits and C3 [complement component 3] traces were detected by immunofluorescence in the choroid plexus of most mice from day 9. Renal lesions included congestion, plugging of veins and capillaries, low-grade mononuclear infiltration and mesangial thickening; these changes were most marked in CBA, C57Bl and A/J mice. Glomerular IgM deposits were present in all strains in the 1st wk of infection. IgG and C3 were detected in the 2nd week, but only traces were found in CBA mice. The livers showed congestion, accumulation of pigment in swollen Kupffer cells and mononuclear portal infiltration; these were most pronounced in A/J mice. In the spleen, there was a great increase in the reticuloendothelial cell population, white pulp proliferation, congestion and accumulation of pigment and plasma cell reaction; the pattern of white pulp expansion varied in the different strains. Apparently, cerebral lesions play a significant role in the acute death etiology in this malaria model.