Another disease caused by a protozoan is malaria, and its vector is a mosquito belonging to genus anopheles. It is the infected female anopheles mosquito which transmits the disease by its bite.
Malaria is a protozoan infection characterized by paroxysms of chills, fever, and sweating, and by anemia, splenomegaly, and a chronic relapsing course.
Malarial parasites are of four types, each with different biologic pattern, may affect man: Plasmodium vivax, P. falciparum, P. malariae, and P. ovale. Infection occurs through the bite of an infected female anopheles mosquito, transfusion of blood from an infected donor, or the use of a common syringe by drug addicts.
The life cycle of the malarial parasite begins when a female anopheles mosquito, feeding on a patient with malaria, ingest blood containing gametocytes. These gametocytes undergo sexual development within the mosquito, to end as sporozoites located in the insect’s salivary glands. The mosquito injects the sporozoites into man, and the parasite multiplies asexually in the liver parenchymal cells. After a period of maturation ranging from days to months, merozoites are released and they invade the red blood cells, initiating the clinical or erythrocytic phase of the disease. If untreated, the infection will last from months to years and produce recrudescent clinical disease. All four types of malaria multiply asexually within the red blood cells, schizogony, to produce new generation of merozoites. The red blood cells rupture and these merozoites are released into the circulating plasma to enter intact red blood cells and repeat the erythrocytic cycle. The urine of the patient becomes reddish due to the ruptured red blood cells.
After prolonged untreated malarial infection or repeated relapses, persistent hepatosplenomegaly develops. The spleen is usually soft and full of malarial pigments. The sinusoids are filled with parasitized red blood cells and the macrophages contain ingested malarial pigments. There are no changes in other organs except the presence of some scattered malarial pigments. The Kupler cells may be distended with parasites and pigments in the macrophages. In fatal falciparum malaria, however, the brain is slate gray and punctate hemorrhages are often scattered throughout the brain substance. The capillaries are choked with parasite-infected red blood cells.
The incubation period is usually 10 to 35 days, often followed by a short prodromal stage characterized by irregular low-grade fever, malaise, headache, myalgia, and chilly sensations that is frequently misdiagnosed as influenza. In vivax and ovale malaria, the primary attack begins abruptly with a shaking chill, followed by fever and sweats with irregularly remittent fever. Within a week, the typical paroxysmal pattern of the disease is established. The initial chill may be preceded by a short period of malaise or headache. The fever may last from one to eight hours, and after it subsides, the patient feels well until the next rigor. The rigors occurs every 48 hrs. in vivax malaria. In falciparum, there may be a chilly sensation rather then a shaking chill, the temperature rises gradually and falls by lysis. The paroxysms may last 20 to 36 hrs. and there is more prostration than in vivax. In falciparum malaria, fever of 40 degrees centigrade and severe headache , drowsiness, delirium, confusion, or parasitemia in excess of 100,000 organisms per cu mm may indicate impending cerebral malaria.
Treatment involves the use of chloroquine phosphate 500 mg taken orally once a week and for children 5mg/kg orally once a week. For resistant cases, a combination of pyramethamine and sulfadoxine is given.
