Detection of Plasmodium falciparum chloroquine resistance transporter (PfCRT) mutant gene amongst malaria-infected pregnant women in Calabar, Nigeria

Chemotherapy is the mainstay in malaria control and management. For some time, chloroquine (CQ) was a drug of choice for the treatment of malaria. It was effective against all forms of malaria, cheap and readily available. The increased resistance of malaria parasites to CQ led to widespread abandonment of the drug in African and Asian countries on the prompting of the World Health Organization. Currently, artemisinin-based combination therapy is the gold standard for the treatment of malaria. This study investigates the presence of the Plasmodium falciparum Chloroquine Resistance Transporter (PfCRT) mutant gene, a molecular marker responsible for CQ resistance in malaria parasites. A total of 369 pregnant women were microscopically screened for malaria infection using thin and thick blood films stained with Giemsa. Subsequently, malaria parasite DNA was extracted from the blood of malaria positive participants. The PfCRT gene was amplified using Polymerase Chain Reaction (PCR). A Restriction Fragment Length Polymorphism analysis of the gene was performed to confirm mutant forms. The results showed that 251 (68.0%) of the participants had Plasmodium falciparum in their blood. Molecular examination revealed the presence of PfCRT mutant genes in 28% of the study population. Notwithstanding the decline in the prevalence of PfCRT T76 mutation since the antimalarial policy change in Nigeria, the 28% prevalence recorded in this study is considered high after ten years of the withdrawal of CQ in the treatment of uncomplicated malaria.