The Fever: How Malaria Has Ruled Humankind for 500,000 Years Read Online Free PDF Page A

out the winter. Later, activated by some as-yet-unknown trigger, the hypnozoite awakens, and the parasite restarts its development and its invasion of red blood cells. (The resulting attacks of malaria suffered by the victim are considered relapses, as opposed to new infections.) This adaptation allowed
P. vivax
to lie low until the bugs started biting again and its blood feasts could resume. 38
    We know that
P. vivax
’s burden must have been costly in Europe and Asia, because genetic mutations that lessened its toll emerged and spread among malaria’s prey, albeit weakening those who carried them. Normally, genes that deform people’s red blood cells impose enough of a disadvantage to their carriers that the gene slowly dies out, and yet in many regions of the world, such deformities persisted and spread. Hemoglobin E, a gene that deforms hemoglobin, slowed
P. vivax
’s progress in the body. A genetic condition called thalassemia reduced people’s risk of getting sick from
P. vivax
infection. Another called ovalocytosis makes red blood cells oval and so rigid that they resist invasion by malarial parasites. Thanks to
P. vivax
, hemoglobin E spread throughout Southeast Asia, thalassemia in the Middle East and Mediterranean, and ovalocytosis through the Pacific region. 39
    But vivax malaria, in its post-Africa incarnation, was not a killer. Rather, it enslaved its victims, imposing a constant and unrelenting tax in blood. The convulsions of fever and chills arrived every summer and fall, as soon as the first mosquitoes fed on the blood of an obliviously relapsing carrier of dormant parasites.
P. vivax
infected the placentas of growing fetuses. Infected babies withered, with stunted immune defenses that rendered them vulnerable to diarrhea and pneumonia. Under the spell of chronic vivax infection, grown men and women weakened to the point that their ambitions drained away and they became anemically prone and wan, just vital enough to make more blood cells available for a later parasitic feed.
    Convulsed by much more dramatic pathogens such as cholera, measles, and smallpox, malaria’s victims may have barely noticed the parasite’s toll. 40 The agrarian lifestyle they had come to lead—staying put on their fetid lands, weak from hunger, living together cheek by jowl—favored the spread of infectious diseases of every ilk.
    Unlike the battle between
P. vivax
and the Duffy gene in Africa, which ended with
P. vivax
’s retreat, the battle between the hemoglobin-deforming genes and
P. vivax
in Europe, Asia, and the Pacific region resulted in one of
P. vivax
’s greatest victories. 41 The malaria parasite had created a new kind of mildly hobbled human, one who could withstand its invasions indefinitely.
    Meanwhile, new opportunities arose in Africa.
    For thousands of years after the Duffy gene beat
P. vivax
out of Africa, the continent probably carried a fairly light burden from malaria. Its nomadic tribes would have encountered malaria-carryingmosquitoes only occasionally. Common ones, such as
Anopheles arabienses
, lived on Africa’s dry savannahs, and fed mostly on animals, not humans. The
Plasmodium malariae
parasite hung on, but just barely, as did an even rarer human malaria parasite,
Plasmodium ovale
.
    But with the formation of the Sahara desert about twenty-five hundred years ago and the spread of Bantu-speaking peoples into the equatorial rain forests of the continent, humankind and mosquitoes collided together in novel ways. The Bantu hacked into the rain forests to grow yams and plaintains, thus transforming those areas. As the trees fell, the chimps and birds disappeared. For the first time, shafts of sunlight reached the rain-forest floor and it became denuded of the thick absorbent layer of humus that once blanketed it. Rainwater collected in puddles on its rutted surface. 42
    A new species of
Anopheles
mosquito emerged to exploit these new ecological conditions, one that constantly, ingeniously, tests out