A growing public health risk originating in Asia, drug resistance, is threatening to undermine gains in malaria control
Significant progress has been made in recent years in the fight against malaria. Since 2000, mortality from malaria has decreased by over 25 percent globally. Scale-up of effective malaria interventions, including the use of artemisinin-based combination therapies – the most effective drug for treating the disease – have been instrumental to this success. However, growing resistance to artemisinins by the malaria parasite has been emerging in Southeast Asia and is threatening to reverse the gains that have been made to date. In this interview, Senior Technical Officer at Malaria Consortium, Dr Prudence Hamade, explains how dangerous a spread the spread of parasite resistance to anti-malarial drugs could be in Asia and beyond.
Q: Can you explain what drug-resistant malaria is and what the state of resistance is now in Southeast Asia?
A: Drug-resistant malaria refers to the strain of malaria parasites that have begun to show resistance to the drug currently being used to kill them. It occurs when a parasite is exposed to a specific drug, often over a long period of time, and successfully changes itself to avoid being killed. Increasingly over the last two or three years, we have noticed that artemisinin, the most effective drug we’ve ever had against malaria, is not working as well as it was in the early days, especially in Asia. It is used in combination with a partner drug, so the treatment is known as artemisinin-based combination therapy or ACT. The drugs clear the parasite from the blood very quickly, which in turn reduces the window for transmission of the parasite from one person to another. ACTs still cure the majority of people within 28 days, but in certain parts of Southeast Asia, there is more and more evidence that the parasite is surviving for longer, which indicates that resistance to artemisinin is on the rise.
Q: Where exactly are the problem areas?
A: The major hotspot for resistance to artemisinin is on the Thai-Cambodia border, where resistance was first detected in 2008. It has since been found elsewhere in Asia: on the Thai-Myanmar border and more recently in Vietnam. Although resistance in these areas is not at the levels we are witnessing along the Thai-Cambodia border, it is a clear indication that resistance to artemisinin is on the rise in the region.
Q: Why is Asia referred to as the hotspot for anti-malarial drug resistance?
Resistance to some of the most effective anti-malarial drugs we have used in the past first emerged in Southeast Asia: resistance to chloroquine for example was detected in the 1950s and Sulphadoxine-Pyrimethamine in the 1990s. Resistance to these drugs is now widespread throughout the world in many malaria endemic countries. Why Southeast Asia is the origin of this resistance is not completely clear but has been linked to the fact that artemisinin was introduced earlier there than elsewhere. Issues around the regulation of antimalarial drugs in the region and the use of monotherapies (where artemisinin is used alone rather than in combination treatments) have also been identified as likely contributors.
Q: The number of cases of malaria in Asia is much lower than in sub-Saharan Africa. Why then is artemisinin resistance in Asia such a grave public health concern?
A: If artemisinin was to stop working in Asia, it would mean that the number of cases of malaria in Asia would increase and become much more serious – because we won’t be able to reduce transmission or treat cases as effectively as before – and mortality will increase. The real worry is that this resistance could spread to Africa (where almost 600,000 people died from malaria in 2010), perhaps transferred by migrants, or emerging spontaneously. At the moment, we are still a long way from having another anti-malarial drug that is as effective or tolerated as well by patients as ACTs. It would then be highly likely that we would see an increase in morbidity and mortality from the disease.
Q: So how serious is the potential spread of resistance from Asia to Africa?
A: When resistance to chloroquine spread to Africa in the 80s and 90s, there were not adequate surveillance systems in place and it took a long time to detect. As a result there was an increase in the number of people dying from malaria. Pregnant women and young children in Africa are particularly vulnerable to malaria because they are the most likely to have either low or no immunity to the diseases, so if resistance to artemisinin were to spread to Africa now or in the next couple of years, the number of deaths among these groups in particular are likely to rise. It would also be more difficult to contain the spread of artemisinin resistance in Africa because of the widespread nature of the disease.
Q: What needs to be done to stop the spread of resistance in Asia?
A: The best case scenario would be to eliminate malaria from the region entirely. That would be extremely complicated but it could be possible. The first step to controlling the spread of resistance is to improve surveillance. We need good reporting systems in place because we need to know where the resistant malaria parasites are located in order to treat and eliminate the drug-resistant strains from those patients. That is the only way to stop the resistant strain spreading: to eliminate the resistant parasites as rapidly as possible by curing the patient quickly, thereby reducing the chances of those parasites being transmitted via mosquitoes to other people.
Q: So what is happening now?
A: The Bill & Melinda Gates Foundation funded the Containment Project, the first major initiative to contain artemisinin resistance in Southeast Asia. This project brought together regional governments and partners, including Malaria Consortium, to develop and implement a multi-pronged strategy to contain the resistance. Now, with support from the Global Fund and AusAid, partners in the region are trying to move beyond containing malaria and resistance, to eliminating malaria from the region altogether.