found in warm low, marshy countries the world over, is caused by protozoan parasites of the family Plasmodiidae which are carried by female anopheline mosquitoes.
There are four species of human malaria: Plasmodium vivax, causing vivax (benign tertian) malaria, Plasmodium malariae, causing quartan malaria, Plasmodium falciparum, causing falciparum (estivo-autumnal) malaria, and Plasmodium ovale, causing a mild tertian malaria. Plasmodium vivax and Plasmodium falciparum have the highest incidence, but contrasting characteristics. Vivax malaria has a 48-hour cycle, is chronic, and tends to relapse in milder forms. Falciparum malaria is often acute and fatal. Diagnosis is made when malarial parasites are found in the blood.The life cycle of the parasite has two aspects, the sexual cycle found in the mosquito and the asexual cycle found in man. The sexual cycle (sporogony), lasting 8 to 10 days in tertian and 10 to 12 in falciparum malaria, begins when an anopheline mosquito biles a carrier of malaria. The mosquito ingests sexual forms which migrate to the stomach where they mature and are fertilized. The resulting zygote burrows into the submucosa of the stomach and becomes encysted (oocyst) and sporulates. The oocyst ruptures releasing sporozoites which migrate through the tissues of the mosquito; especially to the salivary glands. The asexual or human cycle (schizogony) begins when (the infected mosquito bites man and the sporozoites are injected into the blood. After an exoerythrocytic period of about ten days, new forms appear and enter the red blood cells; Plasmodium vivax comes to fill the greater part (up to one third) while Plasmodium falciparum occupies about one-fifth of the cell. Within the next 48 hours in Plasmodium vivax the nucleus divides into numerous small merozoites. The erythrocytes rupture and these merozoites are released into the blood to enter new cells. Sporulation takes place in Plasmodium falciparum irregularly every 36 to 48 hours. The chill or paroxysms occur at this point, once the cycle has become fully established. Just before, during, or shortly after onset of the paroxysm accompanied by chills and high fever, the parasites will be found in blood smears. After several asexual generations, gametocytes (sexual forms) appear.
The injurious effects of malaria result from the destruction of erythrocytes giving rise to hemolytic anemia and also from the liberation of toxic material and pigment and the thrombotic occlusion of arterioles and capillaries. The spleen early in the disease is enlarged, soft and congested, with parasitized red cells. It may rupture during the acute phase. Later the spleen is smaller, firm, slate-gray and contains pigment granules in macrophages. The malarial pigment (hematin) is derived from the hemoglobin of the parasitized red blood cell.The liver goes through changes similar to those in the spleen. There is first engorgement of the hepatic sinusoids with parasitized erythrocytes. Later there is proliferation and enlargement of the Kupffer cells which phagocytize large amounts of pigment. The bone marrow shows deposition of pigment and parasites, an increase of macrophages and erythroblastic hyperplasia.
Changes in the brain are found in falciparum malaria. The cerebral capillaries are dilated and filled with parasitized red cells. Injured capillaries are surrounded by a ring of hemorrhage with an intervening rim of undamaged brain tissue. The capillary in jury is thrombotic, not embolic. Later, the brain tissue surrounding the injured capillary undergoes necrosis and gliosis.
BLACK WATER fever, a rare but often fatal complication of malaria, is caused by a severe hemolytic crisis which is accompanied by jaundice and hemoglobinuria. The renal complications of black water fever are a form of lower nephron nephrosis .
