Heterologous synergistic interactions in concurrent experimental infection in the mouse with Schistosoma mansoni, Echinostoma revolutum, Plasmodium yoelii, Babesia microti, and Trypanosoma brucei.

Primary infections with Plasmodium yoelii and Echinostoma revolutum in the mouse induced a significant increase in the heterologous Schistosoma mansoni challenge worm establishment, whereas S. mansoni worm establishment remained unaffected by primary infections with Trypanosoma brucei and Babesia microti. Concurrent infection in the mouse with P. yoelii or T. brucei, but not with B. microti, blocked the resistance to homologous E. revolutum challenge infection, and primary P. yoelii and T. brucei infections and corticosteroid treatment made naive, innately resistant mice susceptible to E. revolutum infection. Innate resistance to infection with E. revolutum, the pattern of expulsion of low-level E. revolutum infections, and resistance to homologous S. mansoni challenge infection remained unaffected by concurrent B. microti infection. Primary, heavy E. revolutum infections in the mouse resulted in the enhancement of subsequent infection with B. microti, whereas primary infection with S. mansoni suppressed subsequent B. microti infection in some but not all experiments. In a single experiment, P. yoelii infection was suppressed markedly by primary S. mansoni infection, whereas the enhancement of P. yoelii infection in concurrently E. revolutum-infected mice was seen in only one of the several experiments conducted. However, no interference with resistance to homologous B. microti and P. yoelii challenge infection was induced by concurrent infection with S. mansoni and E. revolutum. We suggest that the synergistic interactions demonstrated between protozoans and helminths in concurrent experimental infection in the mouse are induced by immunosuppression.