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Bacillus Calmette-Guérin (BCG) infection of the spleen is a potent modifier of splenic function. Prior to malaria infection, we infected two mouse strains of differing susceptibility to Plasmodium chabaudi AS (C57BL/6 and A/J) with this mycobacterium. We then evaluated aspects of spleen cell composition, architecture and cytokine expression, and correlated these with the outcome. BCG preinfection resulted in protection of the A/J mice but paradoxically resulted in mortality of the C57BL/6 mice. The latter developed higher parasitaemias that peaked earlier than the A/J mice rendered resistant by BCG. BCG infection induced remarkable changes to splenic histology examined by H&E staining, but there were no consistent differences between mouse strains. C57BL/6 mice had higher absolute numbers of all immune cell phenotypes than did A/J mice, and higher macrophage and dendritic cell proportions. BCG-induced resistance in A/J mice was associated with an increased CD4+ expression of IFN-gamma whilst induced death in C57BL/6 mice was associated with excessive IFN-gamma expression. A moderate TH1 response in the A/J model may have been responsible for the improved survival, and an excessive TH1 response in the C57BL/6 model may have contributed to their death.

Original publication




Journal article


Parasite immunology

Publication Date





1 - 12


Department of Veterinary Tropical Diseases, Onderstepoort, South Africa.


Spleen, B-Lymphocyte Subsets, T-Lymphocyte Subsets, CD4-Positive T-Lymphocytes, Macrophages, Animals, Mice, Inbred A, Mice, Inbred C57BL, Mice, Plasmodium chabaudi, Mycobacterium bovis, Parasitemia, Malaria, Splenomegaly, BCG Vaccine, Female, Interferon-gamma