less malaria, although these areas are prone to epidemic malaria if climactic conditions become favorable to mosquito development (World Health Organization, 1996a). Although urban areas have typically been at lower risk, explosive unplanned population growth has been a major factor in making urban or peri-urban transmission an increasing problem (Knudsen and Sloof, 1992).

Human malaria is caused by one or more of four parasites: Plasmodium falciparum, P. vivax, P. ovale, and P. malariae. Distribution of these parasites varies geographically, and not all species of malaria are transmitted in all malarious areas. P. falciparum, the species most commonly associated with fatal malaria, is transmitted at some level in nearly all areas where malaria occurs. It accounts for over 90 percent of all malaria infections in sub-Saharan Africa, for nearly 100 percent of infections in Haiti, and causes two-thirds or more of the malaria cases in Southeast Asia. P. vivax is a relatively uncommon infection in sub-Saharan Africa. Duffy antigens, which are required by the parasite to invade red blood cells, are lacking in many ethnic groups, especially in West Africa. Vivax malaria, however, is the predominant species in Central America, most of malarious South America, and the Indian subcontinent (Miller et al., 1977).

MECHANISMS OF INFECTION AND TRANSMISSION

Malaria is typically transmitted by the bite of an infective female Anopheles mosquito; transmission can also occur transplacentally, as a result of blood transfusion, or by needle sharing. Infective mosquitoes inject sporozoites into the bloodstream during feeding (see Figure 3-1). These sporozoites infect liver cells (b) where they undergo asexual reproduction (exoerythrocytic schizogony), producing schizonts (c). In 6 to 14 days (sometimes longer), the schizonts rupture, releasing merozoites into the bloodstream (d). Merozoites invade red blood cells and undergo a second phase of asexual reproduction (erythrocytic schizogony), developing into rings (e), trophozoites (f), and finally blood stage schizonts (g). The schizonts rupture, destroying the red blood cell and releasing more merozoites into the bloodstream, starting another cycle of asexual development and multiplication (h). This erythocytic cycle will continue until the infected individual is successfully treated, mounts an immune response that clears the infection, or dies. During this cycle, sexual forms called gametocytes are produced (i) and can be ingested by a mosquito during a



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