Experiment in semi-natural conditions did not confirm the influence of malaria infection on bird attractiveness to mosquitoes.

BACKGROUND: Changes in host phenotype following parasite infection are often considered as host manipulation when they seem advantageous for the parasite. However, putative cases of host manipulation by parasites are rarely tested in field-realistic conditions. Infection-induced phenotypic change cannot be conclusively considered as host manipulation if no evidence shows that this trait is adaptive for the parasite in the wild. Plasmodium sp., the parasites causing malaria in vertebrates, are hypothesized to "manipulate" their host by making their odour more attractive to mosquitoes, their vector and final host. While this is fairly well supported by studies on mice and humans, studies focusing on avian malaria give contradictory results. METHODS: In the present study, genotyped birds at different stages (uninfected, acute and chronic) of Plasmodium relictum infection were exposed, in a large outdoor aviary, to their natural vector, the mosquito Culex pipiens. RESULTS: After genotyping the blood meals of more than 650 mosquitoes, we found that mosquitoes did not bite infected birds more than they bit them before infection, nor more than they bit uninfected hosts. CONCLUSIONS: Our study highlights the importance of testing ecological behaviours under natural conditions and suggests that different processes might be at play in mammals and birds regarding potential manipulation of attractiveness by malaria parasites.

Different distribution of malaria parasite in left and right extremities of vertebrate hosts translates into differences in parasite transmission.

Malaria, a vector-borne disease caused by Plasmodium spp., remains a major global cause of mortality. Optimization of disease control strategies requires a thorough understanding of the processes underlying parasite transmission. While the number of transmissible stages (gametocytes) of Plasmodium in blood is frequently used as an indicator of host-to-mosquito transmission potential, this relationship is not always clear. Significant effort has been made in developing molecular tools that improve gametocyte density estimation and therefore prediction of mosquito infection rates. However a significant level of uncertainty around estimates remains. The weakness in the relationship between gametocyte burden, measured from a blood sample, and the mosquito infection rate could be explained by a non-homogeneous distribution of gametocytes in the bloodstream. The estimated gametocyte density would then only be a single snapshot that does not reflect the host infectivity. This aspect of Plasmodium infection, however, remains largely neglected. In both humans and birds, we found here that the gametocyte densities differed depending on which side of the body the sample was taken, suggesting that gametocytes are not homogeneously distributed within the vertebrate host. We observed a fluctuating asymmetry, in other words, the extremity of the body with the highest density of parasites is not always the same from one individual to another. An estimation of gametocyte density from only one blood sample, as is commonly measured, could, therefore, over- or underestimated the infectivity of gametocyte carriers. This might have important consequences on the epidemiology of the disease since we show that this variation influences host-to-mosquito transmission. Vectors fed on the least infected body part had a lower parasite burden than those fed on the most infected part. The heterogeneous distribution of gametocytes in bloodstream should be considered to improve diagnosis and test new malaria control strategies.