Self-medication and Anti-malarial Drug Resistance in the Democratic Republic of the Congo (DRC): A silent threat

Background Malaria is a global infectious (vector-borne: Anopheles mosquitoes) disease which is a leading cause of morbidity and mortality in Sub-Saharan Africa (SSA). Among all its parasitic (protozoan: Plasmodium sp.) variants, Plasmodium falciparum (PF) is the most virulent and responsible for above 90% of global malaria deaths hence making it a global public health threat. Main context Despite current front-line antimalarial treatments options especially allopathic medications and malaria prevention (and control) strategies especially governmental policies and community malaria intervention programs in SSA, PF infections remains prevalent due to increased antimicrobial/antimalarial drug resistance caused by several factors especially genetic mutations and auto(self)-medication practices in SSA. In this article, we focused on the Democratic Republic of Congo (DRC) as the largest SSA country by bringing perspective into the impact of self-medication and antimalarial drug resistance, and provided recommendation for long-term improvement and future analysis in malaria prevention and control in SSA. Conclusions Self-medication and anti-malarial drug resistance is a major challenge to malaria control in DRC and sub-Saharan Africa, and to achieve sustainable control, individual, community and governmental efforts must be aligned to stop self-medication, and strengthen the health systems against malaria

Gentamicin and magnesium chloride normalizes cholinesterase and ATPase activities in rats acutely exposed to dichlorvos (DDVP) pesticide

This study investigated possible use of gentamicin and magnesium chloride as antidotes of dichlorvos pesticide poisoning. Thirty albino rats were randomly divided into 5 groups (n = 6). Group 1 served as negative control and received distilled water only. Group 2 served as positive control and was treated with 2.5 mg/kg body weight dichlorvos intraperitoneally. Group 3 was post-treated with 0.5 mg atropine following intraperitoneal 2.5 mg/kg dichlorvos while groups 4 and 5 rat were post-treated with 28 mg/kg intramuscular magnesium chloride and 5 mg/kg intramuscular gentamicin respectively following intraperitoneal 2.5 mg/kg dichlorvos. Plasma and red blood cell acetylcholinesterase activities were estimated. Total ATPase, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase activities were estimated in the brain. Results showed significant (P < 0.05) increase in acetylcholinesterase activities in rats post treated with Atropine, MgCl2 and Gentamicin when compared with acetylcholinesterase activities in rats treated with dichlorvos only. There is significant (P < 0.05) increase in the activities of Ca2+,Mg2+-ATPases, Na+/K+-ATPase and total ATPase activities in the brain of rats post treated with atropine, magnesium chloride and gentamicin. Dichlorvos significantly (P < 0.05) reduced plasma and red blood cell cholinesterase activities, and brain ATPases activities. We concluded that dichlorvos toxicity inhibited cholinesterase, Na+/K+-ATPase and Ca2+,Mg2+-ATPases activities. Magnesium chloride and gentamicin on the other hand reduced effects of dichlorvos poisoning by promoting normal ATPase activities and inhibiting release of acetylcholine from cell. We proposed that both magnesium chloride and gentamicin can be co-administered in future as antidotes to patients with dichlorvos poisoning