infectious diseases
Malaria
Pathophysiology of Malaria
ThePlasmodiumspecies that infect humans are P. falciparum P. vivax P. ovale P. malariae P. knowlesi Concurrent infection with more than onePlasmodiumspecies is uncommon but can occur. P. knowlesiis a pathogen in Southeast Asia, particularly in Malaysia. Macaque monkeys are the primary hosts.P. knowlesiis usually acquired by people living or working near or in forests. The basic elements of the life cycle are the same for allPlasmodiumspecies. Transmission begins when a femaleAnophelesmosquito feeds on a person with malaria and ingests blood containing gametocytes. During the following 1 to 2 weeks, gametocytes inside the mosquito reproduce sexually and produce infective sporozoites. When the mosquito feeds on another human, sporozoites are inoculated and quickly reach the liver and infect hepatocytes. The parasites mature into tissue schizonts within hepatocytes. Each schizont produces 10,000 to 30,000 merozoites, which are released into the bloodstream 1 to 3 weeks later when the hepatocyte ruptures. Each merozoite can invade a red blood cell (RBC) and there transform into a trophozoite. Trophozoites grow, and most develop into erythrocyte schizonts; schizonts produce further merozoites, which 48 to 72 hours later rupture the RBC and are released in plasma. These merozoites then rapidly invade new RBCs, repeating the cycle. Some trophozoites develop into gametocytes, which are ingested by anAnophelesmosquito. They undergo sexual union in the gut of the mosquito, develop into oocysts, and release infective sporozoites, which migrate to the salivary glands. WithP. vivaxandP. ovale(but notP. falciparumorP. malariae), tissue schizonts may persist as hypnozoites in the liver for years. Relapse ofP. ovalehas occurred as late as 6 years after an episode of symptomatic malaria, and the infection was transmitted by blood transfusion from a person who was exposed 7 years before donating blood. These dormant forms serve as time-release capsules, which cause relapses and complicate chemotherapy because they are not killed by most antimalarial drugs, which typically act on bloodstream parasites. The pre-erythrocytic (hepatic) stage of the malarial life cycle is bypassed when infection is transmitted by blood transfusions, by sharing of contaminated needles, or congenitally. Therefore, these modes of transmission do not cause latent disease or delayed recurrences. Rupture of RBCs during release of merozoites is associated with the clinical symptoms. If severe, Overview of Hemolytic Anemia causes anemia and jaundice, which are worsened by phagocytosis of infected RBCs in the spleen. Anemia may be severe in Unlike other forms of malaria,P. falciparumcauses microvascular obstruction because infected RBCs adhere to vascular endothelial cells. Ischemia can develop with resultant tissue hypoxia, particularly in the brain, kidneys, lungs, and gastrointestinal tract. Hypoglycemia and lactic acidosis are other potential complications. in RBCs is retarded in patients with Sickle Cell Disease , Previous infections provide partial immunity. Once residents of hyperendemic areas leave, acquired immunity wanes over time (months to years), and symptomatic malaria may develop if they return home and become reinfected. 