Gene mutation in malarial parasites causing drug-resistance are not passed onto their offspring

According to the World Health Organization (WHO), about 3.2 billion people are at risk for malaria. Plasmodium species that causes malaria can develop genetic tolerance to antimalarial drugs and this is precisely the reason why it is difficult to eradicate.

According to the World Health Organization (WHO), about 3.2 billion people are at risk for malaria. Plasmodium species that causes malaria can develop genetic tolerance to antimalarial drugs and this is precisely the reason why it is difficult to eradicate.

According to the World Health Organization (WHO), about 3.2 billion people are at risk for malaria. Plasmodium species that causes malaria can develop genetic tolerance to antimalarial drugs and this is precisely the reason why it is difficult to eradicate. Luckily, according to a recent scientific study of a research team from the University of Melbourne led by Dr. Christopher Goodman and Professor Geoffrey Mcfadden, this resistance is not passed onto their offspring.

Atovaquone, an antimalarial drug and an ingredient in the antimalarial medication called Malarone, disrupts the lifecycle of the parasite while living inside their mosquito hosts. It was introduced in 2000 and is known to kill both the blood and liver stages of malarial parasites. This drug is safe for pregnant women and children and was used in mass administration of antimalarial drug. But, the downfall of this drug is that it is prone to resistance which eventually resulted to the stop of its production.


A study on three atovaquone-resistant Plasmodium berghei, a malarial parasite of rodents was conducted to determine whether the drug resistance can be passed on. Each of the strain contains a different mutation on their cytochrome b (cytB) gene that is encoded in their mitochondrial DNA.

 

 

They let Anopheles stephensi mosquitoes to feed on mice infected with and followed what happened to the parasite inside their mosquito hosts. It was found out that while the resistance mutations protect the parasite from the drug, it can be lethal on later stages of the parasite inside the mosquito. Two of the three mutations resulted to developmental defects in the parasite’s fertilized embryos and one led to complete infertility because of damaging female reproductive cells. Thus, rodent malarial parasites with mutations that make them resistant to atovaquone cannot pass this resistance to their offspring. These mutations were called “genetic trap” and can provide a significant step towards our fight against malaria.

Although this study was focused on the rodent malarial parasite, the human malaria parasite, Plasmodium falciparum, also has similar mutations which reduce its ability to successfully infect mosquitoes and also, reduce the number of oocysts produced when infection occurs. This breakthrough made it possible to understand gene mutations that gave rise to drug resistance in some malaria parasite populations and how it kills these parasites in their mosquito hosts. This will then prove helpful in developing drugs that can effectively eliminate malaria and further prevent the spread of drug resistance in malaria parasites.