Etiology

Protozoa assigned to the genus Plasmodium are parasitic in many species of vertebrate animals including birds, reptiles, amphibians, and mammals. Most Old and New World primate species serve as hosts for plasmodia, and some of these parasites are closely related to the species established in human populations. It is generally accepted that the human malaria parasites evolved in association with early human beings, perhaps differentiating into the four species recognized today in the mid-Pleistocene (Garnham 1966; Bruce-Chwatt and Zulueta 1980).

All of the mammalian plasmodia have similar two-phase life cycles: an asexual (schizogonic) phase in the vertebrate host and a sexual (sporogonic) phase in female Anopheles mosquitoes. These cycles reflect ancient anopheline and vertebrate host-parasite relationships that seem to date from at least the Oligocene.

The sexual phase in the mosquito is initiated as the female anopheline takes a blood meal from a human or other vertebrate host. Parasites in ingested red blood cells are released as male and female gametes in the stomach of the mosquito. Fusion of the gametes produces a zygote, which, after rapid development, migrates and encysts in the stomach wall. At maturity, after some 10 to 20 days, this oocyst releases thousands of sporozoites, motile forms that migrate to the salivary glands. When the now infective mosquito bites and probes for vertebrate blood, many of these sporozoites are likely to be injected into the new host in released saliva. The duration of the sexual or sporogonic phase of the cycle is controlled principally by environmental temperature and humidity. P. vivax requires a minimum temperature of 16°C; P. falciparum, at least 18°C. The duration of P. vivax sporogony is 9 to 16 days and that of P. falciparum, 12 to 24 days, when environmental temperatures range between 20° and 25°C (Bruce-Chwatt 1987).

Most of the sporozoites injected by the biting mosquito are phagocytosed, but some, traveling in the bloodstream, reach the liver, enter parenchymal cells, and (as tissue schizonts) proceed by nuclear division to form large numbers (10,000 to 20,000) of merozoites. Eventually, about 6 to 16 days after initial infection, the preerythrocytic schizont ruptures, releasing its merozoites into the bloodstream. Those merozoites that escape phagocytosis invade red blood cells and, as trophozoites, initiate the erythrocytic portion of the asexual phase. The trophozoite form breaks down the hemoglobin of the host erythrocyte, leaving hematin pigment as a digestive product. As it grows, the parasite (now called an erythrocytic schizont) divides, producing 8 to 24 merozoites, depending on the species. For the human malaria parasites, schizogony in the red cell lasts about 48 hours or, for P. malariae, about 72 hours. When the schizont reaches maturity, the erythrocyte bursts and the merozoites are released. Again some will be phagocytosed whereas others will invade uninfected red cells. Erythrocytic schizogony may then continue through repeated cycles with increasing synchronism, manifest as clinical periodicity. As a consequence, more and more red cells are parasitized and destroyed. Immune responses or therapeutic intervention can check the process short of profound anemia, complications, and death.

Following clinical recovery, P. vivax and its close relative P. ovale are capable of causing relapse, even after several years. Recrudescence of quartan malaria (P. malariae infection) may occur after many years, even 30 or more years after initial infection. P. vivax and P. ovale infections can persist because of the survival in the host liver of dormant stages capable of reinitiating erythrocytic schizogony. Recrudes-cent P. malariae infection appears to be due to long-term survival of erythrocytic-stage parasites.

P. falciparum parasites, on the other hand, are much more limited in time of survival; if the disease is left untreated and is not fatal, P. falciparum infection will terminate spontaneously without relapse, usually in less than a year. Instead of developing as trophozoites, small numbers of red cell merozoites differentiate as male and female forms (gameto-cytes). These circulate in erythrocytes and may eventually be ingested by a female Anopheles mosquito -to begin a new sexual phase of the life cycle.

Although malaria transmission normally follows the bite of the infected mosquito, several other routes have been recorded, including congenital transmission and direct transfer of parasites by blood transfusion or by contaminated needles shared by drug abusers. Before the advent of antibiotic therapy, malaria infections were also sometimes induced by injection for therapeutic purposes - for example, to produce high fevers in the treatment of late-stage syphilis.

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