Fighting Malaria: Is our best weapon getting rusty?

Drug resistance is no new thing – you’ve likely heard of MRSA (Methicillin Resistant Staphylococcus aureus) and multi-drug resistant Tuberculosis (MDR-TB). Scientists have developed a host of drugs for treating malaria over the years but these drugs too, have faltered at the hands of the ever-evolving malaria parasites.

study published earlier this week reports on numerous populations in Cambodia of Plasmodium falciparum (one of five malaria species known to infect humans), which often causes severe cases of malaria, that have developed resistance to our most effective post-infection drug treatment to date – artemisinins.  


(The above photo is a picture of “Sweet Wormwood” or Artemisia annua, which contains the active ingredient artemisinin, capable of treating malaria)

Artemisinin resistance is a major global health concern, and the World Health Organisation alongside with Malaria for Medicines Venture and other organisations are collaborating to contain the spread of resistance. If the resistant strains spread and stabilise throughout worldwide malaria parasite populations then we face the risk of artemisinin, our long time reliable malaria treatment, becoming redundant.

Over 200 million people per year get malaria, and in 2010 somewhere between 490,000 and 836,000 people died from it. The drug discovery process is long and arduous, so to have our most effective drug (often used in combination with other drugs such as lumefantrine, amodiaquine or mefloquine for example) at risk of failure to the emergence of resistant strains is not an option for global malaria control.

Caution – Are we certain resistance is emerging?

There have certainly been reports of emerging resistant strains of P falciparum to artemisinin-based combination therapy within the last 4 years in the four countries of the Greater Mekong Subregion of South East Asia (Viet Nam, Cambodia, Thailand and Myanmar). However, many of these reports appear to be isolated incidents and cannot be adequately replicated with further in vivo or in vitro experiments.

For example, field isolates from Africa identified a particular mutation in the gene PfATPase6 (S769N) which coincided with the requirement for a higher dose of artemisinin to clear the malaria parasite. However, only a few of such isolates have been found and subsequently, multiple studies have failed to confirm this S769N mutation in the PfATPase6 gene is responsible for artemisinin resistance, nor being able to identify any gene polymorphisms (singular changes in the nucleotide sequences of a gene) associated with decreased sensitivity to artemisinins in field isolates.

Indeed, there is no unequivocal agreement as to how artemisinins actually work and artemisinins have been tagged as “magic bullets which hit elusive targets”. We have made some progress in recent years to decipher the exact mechanisms of how artemisinins operate, which is promising as we desperately need such information to make reasonable conclusions on whether seemingly resistant strains have in fact emerged as a response to artemisinin use, whether we can counter such resistance by the development of ‘target specific drugs’ and to understand if other factors, beside artemisinin use, are at the hub of this problem.

A recent news blurb from the BBC can be read here.

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