Drug resistance occurs through spontaneous genetic mutations in the parasite. When a patient is treated with a drug (eg, chloroquine), the parasites that are still sensitive to this drug are killed - but other parasites have "mutated" genes which means that they survive.
The mutated parasites survive to reproduce and infect other mosquitoes and, in turn, another person. The parasites with the resistant mutation are thus favoured to survive and reproduce. Several mutations occurring in the same parasite are required to make a parasite resistant to chloroquine, while a relatively small number of mutations are required to make the parasite resistant to sulphadoxine-pyrimethamine (SP, also known as FansidarÃ?®), which is why resistance to SP seems to develop much more quickly than resistance to chloroquine.
Among the factors that increase the likelihood of the survival and transmission of the resistant mutant are failure to complete a course of treatment, poor quality drugs that do not have adequate active ingredient, and clinical diagnosis. The typical malarial symptoms, such as fever, headache and chills, are non-specific to malaria. Basing diagnosis on clinical symptoms without using laboratory tests to confirm the presence of malaria parasites therefore means that many people who do not actually have malaria may end up being treated with antimalarial drugs.
The use of two drugs together, with different mechanisms of action, significantly decreases the likelihood of any one parasite having the mutations required to resist both drugs.
In the 1950s, malaria eradication in Africa was considered impractical