Since allergies serve no good purpose, immunologists could only look on IgE as one of the rare shortcomings of the immune system. But then they discovered that IgE can be good for something: fighting parasitic animals. IgE may be rare in the United States and the few other parts of the world that are now free of intestinal worms, blood flukes, and their like, but the rest of humanity (not to mention the rest of Mammalia) carry a heavy load of flukes, worms, and IgE. Experiments on rats and mice have shown that IgE is crucial for fighting these parasites; if animals are robbed of their IgE, they’re overrun by parasites.
The immune system has, in a sense, recognized that parasitic animals are different from the other creatures that live in our bodies; they’re bigger and their coats are far more complex than those of single-celled organisms. As a result, it has devised a new strategy against them that depends on the IgE antibody. Exactly how that strategy works isn’t completely clear, and it may be a bit different for each parasite. It’s been worked out best for Trichinella, the parasitic worm that grows up in muscle cells and then enters a new host in a piece of meat tumbling into the stomach.
Once Trichinella has thrashed its way free, it moves through its host’s gut by spearing through the projections that line the bowels. Immune cells in the lining of the intestines pick up some of the proteins from the parasite’s coat and travel to the lymph node that lies just behind the intestines. They present the Trichinella proteins to T cells and B cells in the node, setting off the creation of millions of cells targeting the parasite. These B and T cells then come pouring out of the lymph node and swarm through the lining of the intestines.
The B cells make antibodies, including IgE, which spread over the surface of the intestines and form a shield that Trichinella can’t penetrate to anchor itself. At the same time, the mast cells are switched on, bringing on sudden spasms and floods through the intestines. Unable to get any purchase on the intestines, the parasites are washed away.
This precise strategy against a particular parasite—and many others—was in place long before our first primate ancestors swung through the trees 60 million years ago. And if monkeys and apes are any guide today, they needed all the help they could get: primates today are rife with parasites—malaria in their blood, tapeworms and other creatures in their intestines, fleas and ticks in their fur, botflies under their skin, and flukes in their veins.
At some point before 5 million years ago, our own ancestors, living somewhere in Africa, split off from those of today’s chimps. Hominids began standing on two legs and gradually moving from lush jungles to sparser forests and savannas, where they scavenged kills and gathered plants. Some of the parasites of our ancestors followed along with them, branching as their hosts branched into new species. But hominids also picked up new parasites as they shifted to a new ecology. According to Eric Hoberg, they stumbled into the life cycle of tapeworms that beforehand had traveled between big cats and their prey. At the same time, hominids began to spend much of their time at the few watering holes on the savannahs. There they drank from the same water that many other animals did, including rats. A blood fluke that swam from snails to rats stumbled across the skin of a hominid and tried it out. It liked what it found, and gradually a new species of fluke evolved that specialized only in hominids. Ever since then, the fluke Schistosoma mansoni has lived in our veins.
Hominids began moving out of Africa about a million years ago in a series of waves, hiking out across the Old World from Spain to Java. In a popular model of evolution, none of these people have any descendants left on Earth today. Instead, all living humans descend from a final wave that came out of eastern Africa a hundred thousand years ago or so and replaced every other hominid they encountered. On these travels out of the mother continent, our ancestors escaped some parasites. Sleeping sickness depends on tsetse flies to carry trypanosomes, and the flies don’t live outside Africa, so sleeping sickness remained an African disease. But humans also became home to new parasites in their travels. In China, another blood fluke that had been living in rats, Schistosoma japonicum, moved into humans.
At least fifteen thousand years ago, some peoples headed north and east, arcing into the New World through Alaska, and there they encountered a new batch of parasites. The trypanosomes humans had left behind in Africa had existed on that continent for hundreds of millions of years. Before 100 million years ago South America was fused to Africa’s western flank, and the parasites swarmed across the entire landmass. But then plate tectonics tore the two continents apart and poured an ocean between them. The trypanosomes carried away on South America began evolving on their own, into Trypanosoma cruzi and other species. It was long after the split between these two branches of parasites that the first primates evolved in Africa, and for tens of millions of years our ancestors struggled only with sleeping sickness. Humans migrating out of Africa escaped that scourge, but when they finally arrived in South America, the cousins of their old parasites were already there, waiting to greet them with Chagas disease.
By ten thousand years ago, humans had colonized every continent except Antarctica, but they still lived in small groups, eating animals they hunted or wild plants they gathered. Their parasites had to live according to these rules. In those early days, parasites did best if they had reliable routes into humans—tapeworms in big game, for instance, or Plasmodium carried by a blood-hungry mosquito, or blood flukes waiting in the water. Parasites that needed close contact might have brief flashes of glory—Ebola virus racing through a band here or there in central Africa—but the sparseness of humans didn’t allow them to spread beyond that single band, so they remained rare.
That changed when humans began to domesticate wild animals and plants and eat them. The agricultural revolution sprang up independently, first in the Near East ten thousand years ago, then shortly after in China, and a couple of thousand years later in Africa and the New World. Just about every parasite boomed with the dawn of agriculture and the birth of settled towns and cities that followed. Tapeworms didn’t have to wait for humans to scavenge the right carcass or hunt down the right game; they could live in livestock. After humans ate tainted pork and passed tapeworm eggs, it didn’t take long for some snuffling pig to swallow them and let a new generation of parasites begin. By spreading cats and rats around most of the world, humans made Toxoplasma perhaps the most common parasite on Earth. Along the Andes, the houses that Incas built were ideal places for assassin bugs to live, and their llama caravans carried the insect and the parasite across much of the continent. For blood flukes, farming may have been the best thing ever to happen. With people setting up irrigation systems and rice paddies in southern Asia, huge new habitats opened up for the snail hosts of flukes, and the farmers who worked the fields were always in easy reach. Viruses and bacteria could move from person to person in the crowded, dirty conditions in the towns. And faring best of all was Plasmodium. The mosquitoes that carry malaria prefer to lay their eggs in open standing water, and as farmers cleared forests they brought exactly those sorts of pools into existence. The rising swarms of mosquitoes discovered new targets far more easily than their ancestors had: people toiling in fields during the day and clustering in villages at night.