Despite attempts to foil malaria using insecticides and pharmaceuticals, the scourge still infects approximately 300 million people annually and kills as many as 2 million. Now new findings shed further light on why the disease is so hard to control. According to two reports published today in the journal Nature, the malarial parasite Plasmodium falciparum is older and more genetically diverse than previously thought. Moreover, it develops drug resistance surprisingly quickly.
The precise origin and evolution of P. falciparum is the subject of much debate. To trace the parasite's lineage, Jianbing Mu of National Institute of Allergy and Infectious Diseases (NIAID) and colleagues looked for genetic differences among five P. falciparum samples hailing from Southeast Asia, Africa, South America, Central America and Papua New Guinea. Specifically, the team examined so-called single nucleotide polymorphisms (SNPs) from 204 genes on chromosome 3 of the parasites. Based on the differences they found, the team estimates that the most recent common ancestor existed between 100, 000 and 180, 000 years ago. This finding is at odds with the theory that the organism went through a population bottleneck less than 5,000 years ago, which would have left today¿s widely dispersed parasites more closely related. Instead, explains study co-author Xin-zhuan Su of NIAID, the researchers "speculate that when the human population grew, the malaria parasite grew with it."
The second report investigated the parasite's response to a widely used antimalarial drug, chloroquine. Chloroquine-resistant strains of malarial have existed for more than four decades but how this invulnerability arose and its impact on other strains of the parasite remains difficult to assess. John C. Wootton of the National Institutes of Health and his colleagues found that the gene responsible for this resistance, dubbed pfcrt, is in fact widely distributed in parasites from around the world. Using 87 parasite samples from geographically distant patients, the scientists determined that there were at least four distinct resistance-conferring events. In addition, they report that pfcrt moved across continents very quickly, requiring less than 80 generations (between six to 30 years) to become established. The results highlight the need for careful drug-use monitoring programs in current and future attempts to curtail the disease. Notes Su, a member of both research teams, "this means that when a drug- or vaccine-resistant parasite arises, it will not take long for this resistance to spread to other continents, reflecting human travel, particularly by air, and the high transmission rate via mosquitoes in Africa."