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Malaria, caused by parasites of the genus  Plasmodium , leads to over half a million deaths per year, 90% of which are caused by  Plasmodium falciparum .  P .  vivax  usually causes milder forms of malaria; however,  P .  vivax  can remain dormant in the livers of infected patients for weeks or years before re-emerging in a new bout of the disease. The only drugs available that target all stages of the parasite can lead to severe side effects in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency; hence, there is an urgent need to develop new drugs active against blood and liver stages of the parasite. Different groups have demonstrated that triclosan, a common antibacterial agent, targets the  Plasmodium  liver enzyme enoyl reductase. Here, we provide 4 independent lines of evidence demonstrating that triclosan specifically targets both wild-type and pyrimethamine-resistant  P .  falciparum  and  P .  vivax  dihydrofolate reductases, classic targets for the blood stage of the parasite. This makes triclosan an exciting candidate for further development as a dual specificity antimalarial, which could target both liver and blood stages of the parasite.

Plasmodium dihydrofolate reductase is a second enzyme target for the antimalarial action of triclosan