Malaria remains one of the most dangerous infectious diseases in Africa, caused by the Plasmodium parasite and transmitted by female Anopheles mosquitoes. Its infection process is complex, involving both mosquito and human hosts. When an infected mosquito bites a person, it injects sporozoites into the bloodstream. These sporozoites quickly travel to the liver, where they multiply silently for 7–10 days. At this stage, the infected person shows no symptoms. Once thousands of parasites (merozoites) are released from the liver into the bloodstream, they invade red blood cells. Inside the red cells, they multiply and eventually rupture the cells, releasing more parasites. This cycle causes the classic malaria symptoms—fever, chills, body pain, and sweats. Some parasites also develop into sexual forms (gametocytes), which are taken up when another mosquito bites the person, continuing the cycle of transmission. Antimalarial drugs target the blood stage, effectively treating symptoms. However, species like P. vivax and P. ovale also form dormant liver stages (hypnozoites), which most drugs cannot eliminate, leading to relapses. The greater challenge today is drug resistance. Resistance develops when parasites mutate and survive drug treatment. This often occurs due to incomplete treatment, poor-quality drugs, or insufficient dosing. These surviving resistant parasites spread, especially in areas with high drug use and mosquito prevalence. Over time, resistant strains become dominant, making malaria harder and costlier to treat.