Toxoplasma gondii: How an Amazonian parasite became an Inuit health issue.

Toxoplasma gondii is a protozoan parasite that originated in the Amazon. Felids (mammals in the cat family) are the only definitive hosts. These animals shed large numbers of infectious oocysts into the environment, which can subsequently infect many intermediate hosts, including birds, mammals and, possibly, fish. Human T. gondii seroprevalence is high in some parts of the Canadian Arctic and is associated with adverse health consequences among Inuit population. Since the range of felids does not extend to the Arctic, it is not immediately obvious how this parasite got from the Amazon to the Arctic. The objectives of this overview are to summarize the health impacts of T. gondii infection in Inuit in Canada's North and to consider how this infection could have reached them. This article reviews the prevalence of T. gondii infection in terrestrial and marine animals in the Canadian Arctic and discusses their potential role in the foodborne transmission of this parasite to humans. Two distribution factors seem plausible. First, felids in more southern habitats may release infectious oocysts into waterways. As these oocysts remain viable for months, they can be transported northward via rivers and ocean currents and could infect Arctic fish and eventually the marine mammals that prey on the fish. Second, migratory terrestrial and marine intermediate hosts may be responsible for carrying T. gondii tissue cysts to the Arctic, where they may then pass on the infection to carnivores. The most likely source of T. gondii in Inuit is from consumption of traditionally-prepared country foods including meat and organs from intermediate hosts, which may be consumed raw. With climate change, northward migration of felids may increase the prevalence of T. gondii in Arctic wildlife.

Assessment of Plasmodium falciparum PfMDR1 transport rates using Fluo-4.

Mutations in the multidrug resistance transporter of Plasmodium falciparum PfMDR1 have been implicated to play a significant role in the emergence of worldwide drug resistance, yet the molecular and biochemical mechanisms of this transporter are not well understood. Although it is generally accepted that drug resistance in P. falciparum is partly associated with PfMDR1 transport activity situated in the membrane of the digestive vacuole, direct estimates of the pump rate of this transport process in the natural environment of the intact host-parasite system have never been analysed. The fluorochrome Fluo-4 is a well-documented surrogate substrate of PfMDR1 and has been found to accumulate by actively being transported into the digestive vacuole of several parasitic strains. In the present study, we designed an approach to use Fluo-4 fluorescence uptake as a measure of compartmental Fluo-4 concentration accumulation in the different compartments of the host-parasite system. We performed a 'reverse Fluo-4 imaging' approach to relate fluorescence intensity to changes in dye concentration rather than Ca(2+) fluctuations and were able to calculate the overall rate of transport for PfMDR1 in Dd2 parasites. With this assay, we provide a powerful method to selectively measure the effect of PfMDR1 mutations on substrate transport kinetics. This will be of high significance for future compound screening to test for new drugs in resistant P. falciparum strains.