Pathophysiology

The organism is transmitted primarily by the bite of an infected female anopheline mosquito. This vector is most frequently found in tropical and subtropical regions below 8200 ft (2500 m) above sea level. Plasmodial sporozoites are injected into the host's bloodstream during the mosquito's blood meal and are carried directly to the liver. The hepatic parenchymal cells are invaded, and asexual reproduction of the parasite begins (preerythrocytic schizogony or exoerythrocytic stage). As thousands of daughter merozoites are formed, the parenchymal liver cell ruptures, releasing daughter merozoites back into the circulation, where they rapidly invade erythrocytes (erythrocytic stage). In P. vivax and P. ovale infection, a portion of the intrahepatic forms are not released, remain dormant for months, and can later activate and cause clinical relapses.

The clinical manifestations of malaria first appear during the erythrocytic stage. Once merozoites enter this stage, they never reinvade the liver. Merozoites mature within the erythrocyte and take on various morphologic forms, including the early ring forms, trophozoites, and schizonts (which represent a mass of new merozoites). Eventually, the target erythrocyte lyses, and new merozoites invade uninfected red blood cells, continuing the infection and causing clinical manifestations. Lysogeny may become regular, occurring at 2- to 3-day intervals in established and untreated infections, producing the classic periodicity of symptoms.

After several cycles, a proportion of the merozoites develop into sexual forms (gametocytes). Upon ingestion by another feeding anopheline mosquito, male and female gametocytes undergo sexual reproduction and become infective sporozoites ready for their next host.

Each species of Plasmodium has specific characteristics, including typical morphologic forms and selective red blood cell tropism ( XabJ.e,...142-2). Many of these characteristics are responsible for important pathophysiologic consequences.

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