Thursday, February 21, 2013

Evolution of Drug Resistance in Malaria


With only a limited number of drugs currently available to treat or prevent malaria, antimalarial drug resistance has rapidly become the greatest challenge in malaria control today. Resistance typically develops through “spontaneous mutations that confer reduced sensitivity to a given drug” (Bloland 2001). While multiple mutations are required to confer resistance against some drugs, a single point mutation can suffice for others. Malaria infections have been found with widely variable drug susceptibility, ranging from highly resistant to completely sensitive. If the resistance is able to perpetuate, it can become quickly established in a population.
In the 1950s, the drug chloroquine was introduced and heralded as a “miracle cure” against Plasmodium falciparum, the most deadly type of malaria (Fuller 2009). However shortly thereafter, the first resistant strains were reported along the Panama-Colombian and Thai-Cambodian borders, and by the early 1990s, chloroquine was considered ineffective in many parts of the world, including sub-Saharan Africa (Plowe 2008). A number of factors can contribute to the spread of resistance, including vector and parasite biology. Evidence has suggested that certain combinations of drug-resistant parasites and vector species have higher rates of drug resistance transmission than others. In addition, because many antimalarial drugs have similarities in chemical structure, development of resistance to one oftentimes allows for development of further resistance to other drugs, leading to multiple drug resistant (MDR) strains (Bloland 2001).
New treatments incorporating the drug artemisinin has seen promising success in recent malaria treatment, but there is now growing concern that artemisinin is losing its potency (Fuller 2009). Malaria experts have identified early signs of resistance to artemisinin in the same area “around the Thai-Cambodian border” which “appears to have been a starting point” for other drug-resistant strains of malaria, including that of the drug chloroquine. The World Health Organization posits three current viable methods of combating drug resistance in malaria: reducing overall drug pressure with improvements in diagnoses and more rigid prescribing practices, implementation of directly observed therapy (DOT) techniques and other close follow-up approaches to ensure optimal drug use, and combination therapies with a variety of antimalarial drugs.


Bloland, Peter B. "Drug Resistance in Malaria." World Health Organization, 2001. Web. 21 Feb. 2013.

Fuller, Thomas. "Spread of Malaria Feared as Drug Loses Potency." The New York Times. N.p., 27 Jan. 2009. Web. 21 Feb. 2013.

Plowe, Christopher V. "The Evolution of Drug-resistant Malaria." National Center for Biotechnology Information. US National Library of Medicine National Institutes of Health, 12 Dec. 2008. Web. 21 Feb. 2013.

Word count: 352

Sean Kim

7 comments:

  1. So, how does the malaria parasite evolve its resistance? If a single point mutation can confer drug resistance, then I'm guessing that protein structure has a lot to do with the mechanism of infection.

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  2. Rapidly evolving drug resistance, in my opinion, in the biggest obstacle facing the world of medicine today. Did you come about any articles that discussed the possibility of gene therapy to install resistance to malaria in people?
    -Mary Morales

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  3. with an increase in drug resistance? how do you propose we solve the issue?

    What kind of mechanisms are we targeting in the current antibiotics and by what mechanisms are they being retaliated against?

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  4. We're currently attempting to solve the drug resistance problem through combination therapy. The idea is that it is very unlikely for a strain of malaria to evolve resistance against two different drugs. Therefore, the therapy will kill that case of malaria and prevent any secondary infections.

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  5. Directly observed therapy (DOTS) is also widely used to treat tuberculosis. An issue present with this disease is that people begin taking the prescribed drugs to cure TB but when their symptoms go away they stop taking the medication, which leaves only the stronger, more viable pathogens in their body to reproduce and resistant strains of TB. By watching the patients take their medications health care workers ensure that the drugs are taken for the full course of treatment and all pathogens are killed.

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  6. I agree with Mary, who mentioned that the rapid evolution of resistance to drugs is one of the biggest challenges researchers face when trying to eliminate disease - it seems that we are not necessarily at a lack of resources or the "know-how" to cure said diseases, but we are just not at the right state to eliminate them wholly, as clearly we struggle with drug resistance in many different viruses/bacteria, such as HIV or VRSA. With the recent curing of HIV offering global hope, it'll be interesting to trace the progression of new techniques to cure these resistant strains of viruses/bacterias.

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  7. I wonder what it is about diseases like malaria that make them more likely to come up with new strains. Is it a genetic factor that makes malaria more susceptible to mutation than others? Is there a way to control for this type of accelerated rate of mutation?

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