Co-infection with Trypanosoma cruzi protects mice against early death by neurological or pulmonary disorders induced by Plasmodium berghei ANKA

• Published in: Malaria Journal
• Main Authors: Costa Fabio T, Maeda Fernando Y, Cortez Mauro, Covarrubias Charles, Sasso Gisela RS, Macedo Silene F, Egima Claudia M, Yoshida Nobuko
• Format: Article in Journal/Newspaper
• Language: English
• Published: BMC 2007
• Subjects: Arctic medicine. Tropical medicine; RC955-962; Infectious and parasitic diseases; RC109-216; Arctic
• Online Access: https://doi.org/10.1186/1475-2875-6-90; https://doaj.org/article/dff0fbf2821d48f28659f6b1a63efa4c

Abstract Objective The objective of this study was to investigate whether the infection of C57BL/6 mice by P. berghei ANKA, which causes severe malaria, was modulated by co-infection with Trypanosoma cruzi . Methods Groups of C57BL/6 mice were infected either with P. berghei ANKA, T. cruzi strain G, or with both parasites. The presence of parasites was checked by microscopic examination of blood samples. Symptoms of neurological or respiratory disorders, as well as mortality, were registered. Breakdown of the blood brain barrier was determined by injecting the dye Evans blue. Histological sections of the lung were prepared and stained with hematoxilin-eosin. Results All mice infected only with P. berghei ANKA died within 7–11 days post-infection, either with symptoms of cerebral malaria or with respiratory abnormalities. The animals co-infected with T. cruzi strain G survived longer, without any of the referred to symptoms. Protection against the early death by severe malaria was effective when mice were given T. cruzi 15 days before P. berghei inoculation. Breakdown of the blood brain barrier and extensive pulmonary oedema, caused by malaria parasites, were much less pronounced in co-infected mice. The degree of protection to severe malaria and early death, conferred by co-infection with T. cruzi , was comparable to that conferred by treatment with anti-CD8 antibodies. Conclusion Co-infection with T. cruzi protects C57BL/6 against the early death by malaria infection, by partially preventing either the breakdown of the blood brain, and cerebral malaria as a consequence, or the pulmonary oedema.