Andrew Kasiti Muganda^1,, Edward Owiti Okonjo¹, James Nyabuga Nyariki², Dorcas Syokui Yole¹

Malaria is a severe infection caused by the Plasmodium parasite. It causes high mortality and morbidity, especially in the malaria endemic region. Schistosomiasis is caused by blood flukes and is the second leading parasitic infection after malaria in morbidity and mortality rate. These two infections are co-endemic in many areas. Both parasites have definitive and intermediate hosts and each utilizes the host protein differently. Each utilizes the host protein differently. The objective of this study was to determine the outcome of chronic S. mansoni infection in the regulation of Plasmodium berghei ANKA (PbA) associated disease severity and pathological events in a mouse model. Mice were infected with 200 Schistosoma mansoni cercaria and later with 50000 PbA infected red blood cells. Parasitemia was monitored on a two-day interval, to track the infection levels. Furthermore, relative organ weight, and inflammatory markers were quantified at the end of the study and analyzed at a p = 0.05. Chronic S. mansoni infection suppressed PbA parasitemia. Meanwhile, co-infection with S. mansoni and PbA protected against schistosomiasis induced hepatosplenomegaly. Moreover, induction of both schistosomiasis and malaria abrogated PbA induced elevated levels of TNF-α and IFN-γ cytokines, associated with inflammation. Co-infection with S. mansoni and PbA enhanced PbA induced suppression of anti-inflammatory cytokine IL-10. Standard histopathological analysis revealed that when mice were infected with S. mansoni or PbA alone they had pronounced organ damage, which was assuaged by co-infection with both parasites. Findings from this study clearly reveals that co-infection with S. mansoni and PbA, significantly protects mice against either S. mansoni or PbA -driven inflammatory response and organ damage.

schistosomiasis, malaria, co-infection, inflammation, hepatology