Free The Coming Plague by Laurie Garrett Page B

one to three weeks the sac would grow, as inside thousands of sporozoite-stage parasites were manufactured. Eventually, the sac would explode, flooding the insect’s gut with microscopic one-celled parasites that caused no harm to the cold-blooded insect; their target was a warm-blooded creature, one full of red blood cells.
    Some of the sporozoites would make their way into the insect’s salivary glands, from which they would be drawn up into the “syringe” when the mosquito went on her nightly sundown feeding frenzy, and be injected into the bloodstream of an unfortunate human host.
    At that point the speed and severity of events (from the human host’s perspective) would depend on which of four key malarial parasite species had been injected by the mosquito. A good parasitologist in the 1950s knew a great deal about the differences between the four species, two of which were particularly dangerous: Plasmodium vivax and P. falciparum.
    If a human host was most unlucky, the parasites coursing through her bloodstream would be P. falciparum and she would have only twelve days to realize she’d been infected and get treatment of some kind before the disease would strike, in the form of either acute blood anemia or searing infection of the brain. In either case, for an individual whose immune system had never before seen P. falciparum , the outcome would likely be death.
    Scientists knew that injected sporozoites made their way to the liver, where they underwent another transformation, becoming so-called schizonts capable of infecting red blood cells. By the millions the tiny creatures, matured into merozoites, multiplied and grew inside red blood cells, eventually becoming so numerous that the cells exploded. Soon the human body would be severely anemic, its every tissue crying out for oxygen. If the immune system managed to keep the merozoite population down to manageable levels, the results would be prolonged—perhaps chronic lifetime —fatigue and weakness. Unchecked, however, the merozoites would so
overwhelm the red blood cell population that the host’s brain, heart, and vital organs would fail and death would result.
    During the merozoite invasion of the blood supply, a smaller number of male and female gametocyte-stage P. falciparum would also be made, and the entire cycle of events would repeat itself when another female Anopheles mosquito fed on the blood of the ailing human, sucking those gametocytes up into her proboscis.
    Understanding that process of the disease was relatively easy; more difficult was predicting when and why humans and Anopheles mosquitoes were likely to come into fatal contact and how the spread of malaria could be stopped.
    Several types of monkeys were known to serve as parasite reservoirs, meaning that for long periods of time the disease could lurk in monkey habitats. The Anopheles mosquito would happily feed on both the monkeys and the humans that entered such ecospheres, spreading P. falciparum between the species. 17
    The size of Anopheles mosquito populations could vary drastically in a given area, depending on rainfall, agricultural practices, the nature of human housing and communities, altitude, proximity to forests or jungles, economic development, the nutritional status of the local people, and numerous other factors that could affect mosquito breeding sites and the susceptibility of local human populations. 18
    Almost entirely absent in the mid-twentieth century was an intellectual perspective that wedded the ecological outlook of the classical parasitologist with the burgeoning new science of molecular biology then dominating the study of nontropical bacteria and viruses. Money was shifting away from research on diseases like malaria and schistosomiasis. Young scientists were encouraged to think at the molecular level, concentrating on DNA and the many ways it affected cells.
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    Imbued with profound optimism, coupled with the post-World War II