Malaria is an infectious disease that affects millions of people in the developing world. It is responsible for the very high infant mortatlity rate still seen in some countries in Africa. Efforts to control the disease involve interrupting the malaria life cycle by killing the mosquitoes that carry the parasite, usually Plasmdodium falciparum and Plasmodium vivax. When people become infected, drug treatment involves giving malaria tables that usually contain artemisinin combination therapy ACT and other drugs that are far more effective than quinine and chloroquine, but resistance to therapy is an increasing problem.
In Zambia the first-line treatment for uncomplicated malaria is artemisinin combination therapy (ACT). The drug artemether-lumefantrine is most commonly used as an antimalarial. However, the antifolate drug sulphadoxine-pyrimethamine (SP), remains the treatment of choice for malaria in children weighing less than 5 kg and also in pregnant women showing malaria symptoms
This drug can also be used as a preventive therapy in pregnancy to reduce the risk of the woman developing malaria and putting the life of her unborn baby at risk. It also serves as and important stand-by treatment during ACT stock outs. This study investigated how Plasmodium falciparum point mutations were related to antifolate drug resistance in the area around Macha. Mutations in the related parasite plasmodium vivax was not assessed in this particular piece of research
The study involved taking a representative sample of 2,780 residents from the vicinity of Macha and screening them for malaria by microscopy.
At the same time, blood was collected onto filter paper and dried for subsequent Plasmodium falciparum DNA analysis.
Of the 188 people who were found to be infected by the malaria parasite, even though they may not necessarily have been suffering from obvious symptoms of malaria, 95 were chosen for further analysis. The Plasmodium falciparum parasite obtained from each sample was genotyped for DHFR and DHPS antifolate resistance mutations using nested PCR and allele-specific restriction enzyme digestion.
The Plasmodium falciparum field samples exhibited a high prevalence of antifolate drug resistance mutations, including the DHFR triple (Asn-108 + Arg-59 + Ile-51) mutant (41.3%) and DHPS double Gly-437 + Glu-540) mutant (16%). The quintuple (DHFR triple + DHPS double) mutant was found in 4 (6.5%) of the samples.
These results show that the proportion of Plasmodium falciparum with these types of drug mutation is increasing and has shown a dramatic escalation, relative to previous surveys carred out in 1988.
Conclusions: This study points to escalating levels of P. falciparum antifolate resistance in the vicinity of Macha. Continued monitoring is recommended to ensure timely policy revisions before widespread resistance exacts a serious public health toll.
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Author: Mtawa AP Mkulama, Sandra Chishimba, Jay Sikalima, Petrica Rouse, Philip E Thuma and Sungano Mharakurwa
Credits/Source: Malaria Journal 2008, 7:87