Modelling Malaria Control

I n the past ten years, the rich world has begun to get serious about tackling the diseases that predominantly affect poor people, diseases that impose an enormous humanitarian and economic burden upon those least able to bear it. Infections comprise the majority of this burden, and three have been singled out for particular attention: HIV/AIDS, tuberculosis, and malaria. Of these, malaria is probably the easiest to attack. But how should we attack it? Traditionally, we have relied on vector control (killing anopheline mosquitoes) and drug treatment of malaria episodes, and this combined approach has proved remarkably effective in many settings. Malaria is no longer a problem in most of China, Russia, Europe, and North America. But attempts at global eradication foundered in the tropics in the 1960s [1], and we have been reluctant to try again. Waiting for a malaria vaccine has provided one excuse for treading water, but whilst we have waited, malaria morbidity and mortality have worsened [2]. Resistance to the widely available and inexpensive chloroquine and sulphadoxine-pyrimethamine (SP) has been the main culprit [3]. Doing nothing is not an option. Fortunately, we do now have malaria control interventions that work: effective insecticides, insecticide-impregnated materials (particularly bed nets), and highly effective drugs. And there is increasing political will to direct international donor assistance to malaria control. So how should we use the increasing funds available for purchasing malaria control tools to best effect? In particular, how can we prevent or at least delay losing the new antimalarial drugs to resistance? If we are to roll back malaria, we will certainly need to deploy highly effective antimalarial drugs on a much wider scale than we do now. There are some areas of broad agreement, many of which apply more generally to infectious disease treatments. Inadequate dosing must be avoided, fi xed combinations of drugs (as used in the treatment of tuberculosis and HIV/AIDS) should become the norm, and unnecessary overuse should be minimised. When large numbers of malaria parasites are exposed to antimalarial drugs, then spontaneously arising mutants with point mutations or gene amplifi cations that confer reduced drug susceptibility may be selected. This selective pressure is inevitable when slowly eliminated drugs are deployed on a large scale in malaria-endemic areas. Resistance has developed to all currently available classes of antimalarial drugs, with the important exception of the artemisinin compounds. Mass treatment and large-scale prophylaxis with antimalarial drugs …