Multiple infections by parasitic agents that cause diverse clinical manifestations occur frequently and increase or decrease of overall pathogenic impact can be influenced by synergistic or competitive interactions between parasite species [
1,
2]. Malaria is prevalent throughout tropical regions where concomitant infections occur frequently. Double infections with
Plasmodium spp. and
Ascaris lumbricoides, or triple infections with the two parasites plus
Trichuris trichiura, without synergism or antagonism among parasites, have been reported in Zaire [
3]. Concomitant parasitism by agents of malaria and lymphatic filariasis, with no indication of interaction between the two infections, has been detected in India and in Guyana [
4,
5]. On the other hand, it has been found that Senegalese children lightly infected with
Schistosoma haematobium had lower
Plasmodium falciparum densities, suggestive of negative interactions between both parasites [
6]. It has been pointed out that, if worms have in fact deleterious effect on malaria, treatment of helminthic infection would offer an affordable and effective means to roll back malaria [
7]. Experiments in mice have shown that malaria-filaria co-infection causes more severe anaemia and loss of body mass than
Plasmodium chabaudi malarial infection alone [
8], and that concomitant
P. chabaudi and
Schistosoma mansoni infections increase malaria parasitaemia and suppress spleen cell proliferative and Th2 responses to
S. mansoni soluble egg antigen [
9]. Using
Plasmodium berghei ANKA, which causes lethal cerebral malaria in C57BL/6J mice, Legesse
et al. [
10] found that superinfection with
S. mansoni enhanced malaria parasite development, increasing parasitaemia and mortality.
As regards the mixed infection by malaria parasite and another protozoan, the data are sparse. The possibility, for instance, of co-infection with
Trypanosoma cruzi, the agent of Chagas' disease, has not been examined. In Brazil, as there has been an increase in cases of Chagas' disease in the Amazon, where malaria prevails, recommendations have been made to include the microscopic analysis of blood smears for direct search of
T. cruzi in patients with fever in the routine survey for malaria parasites [
11]. Thirty years ago, Krettli [
12] reported that in double infection with
P. berghei NK65 and
T. cruzi about 40% of mice chronically infected with
T. cruzi relapsed to the acute phase when inoculated with
P. berghei, while some decrease in
P. berghei parasitaemia was observed. Since then, the question has not been further addressed. This study aimed at investigating if, and to what extent, the agents of malaria and Chagas' disease exerted their effects to each other's course of infection. To that end,
P. berghei ANKA, which produces cerebral malaria in C57BL/6 mice, and a
T. cruzi strain from the Amazon, which produces subpatent infection, were used.