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Abstract
Malaria remains a significant public health challenge, particularly in tropical and subtropical regions such as Nigeria, prompting global efforts for a definitive cure and complete eradication. The search for a lasting cure and total eradication of malaria has become a major concern of the World Health Organization (WHO). However, antimalarial drug resistance has emerged as one
of the most serious challenges to malaria control today surpassing the pace of new antimalaria drug development.Several concerns have been raised regarding the resistance observed in artemisinin combination therapy (ACT), the predominant treatment for malaria. The efficacy of ACT is been threatened due to reported cases of resistance, and if this resistance spreads, it could pose a significant threat to Africa, where malaria is prevalent. Hence, monitoring the emergence and spread of this resistance is crucial, particularly in malaria-prone regions like Nigeria. This study investigates the possible emergence of Plasmodium falciparum malaria infection resistance to artemisinin combination therapies (ACTs) drugs, currently used in the treatment of malaria in Benin City. Additionally, it examines the expression of the PFK13 gene, which is known for itsassociation with artemisinin resistance.Two categories of artemisinin combination therapy,Lonart(artemether and lumefantrine)and Artequin (artemether and mefloquine),were employed. A cross sectional study of subjects with Lonart resistant malaria and artequin resistant malaria in Benin metropolis was carried out and the resulting resistant effects were documented. Clinical investigation of the artemisinin resistant malaria patients alongside with full blood count parameters such as packed cell volume, white blood cell count, neutrophils, eosinophils and lymphocytes were assessed and compared to a control group. Subsequently, subjects received quinine infusion and injections, and the same parameters were evaluated post-treatment and compared with the control. Gene expression analysis of the PFK13 gene was performed for both Lonart and Artequin-resistant malaria parasite in the blood of the patients with malaria parasite,and the findings were compared with control groups. Results indicated lower packed cell volume and white blood cell values in subjects compared to the control group. However, after treatment with quinine infusion and injection, no significant differences were observed compared to the control group. PFK13 gene expression was higher in Lonart and Artequin-resistant malaria parasite subjects compared to the control groups. The study suggests the potential emergence of artemisinin resistance in Benin City. Nevertheless, further investigations, particularly into PFK13 gene mutations, will provide accurate marker for potential artemisinin resistance.
of the most serious challenges to malaria control today surpassing the pace of new antimalaria drug development.Several concerns have been raised regarding the resistance observed in artemisinin combination therapy (ACT), the predominant treatment for malaria. The efficacy of ACT is been threatened due to reported cases of resistance, and if this resistance spreads, it could pose a significant threat to Africa, where malaria is prevalent. Hence, monitoring the emergence and spread of this resistance is crucial, particularly in malaria-prone regions like Nigeria. This study investigates the possible emergence of Plasmodium falciparum malaria infection resistance to artemisinin combination therapies (ACTs) drugs, currently used in the treatment of malaria in Benin City. Additionally, it examines the expression of the PFK13 gene, which is known for itsassociation with artemisinin resistance.Two categories of artemisinin combination therapy,Lonart(artemether and lumefantrine)and Artequin (artemether and mefloquine),were employed. A cross sectional study of subjects with Lonart resistant malaria and artequin resistant malaria in Benin metropolis was carried out and the resulting resistant effects were documented. Clinical investigation of the artemisinin resistant malaria patients alongside with full blood count parameters such as packed cell volume, white blood cell count, neutrophils, eosinophils and lymphocytes were assessed and compared to a control group. Subsequently, subjects received quinine infusion and injections, and the same parameters were evaluated post-treatment and compared with the control. Gene expression analysis of the PFK13 gene was performed for both Lonart and Artequin-resistant malaria parasite in the blood of the patients with malaria parasite,and the findings were compared with control groups. Results indicated lower packed cell volume and white blood cell values in subjects compared to the control group. However, after treatment with quinine infusion and injection, no significant differences were observed compared to the control group. PFK13 gene expression was higher in Lonart and Artequin-resistant malaria parasite subjects compared to the control groups. The study suggests the potential emergence of artemisinin resistance in Benin City. Nevertheless, further investigations, particularly into PFK13 gene mutations, will provide accurate marker for potential artemisinin resistance.
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