Over the course of tens of millions of years, new kinds of vertebrates evolved on land: upright mammals and reptiles. These animals no longer offered the easy target of a slimy belly hugging the ground—they stood high on tall legs. Some parasitic nematodes adapted to these new hosts by evolving a new entry: by getting eaten rather than burrowing in through the skin. But burrowing, Sukhdeo argues, was too deep in their nature to disappear. Once swallowed, they would take up the flesh-drilling pilgrimage their ancestors had made for millions of years, looping back through their host’s body in order to enter the intestines again.
Sukhdeo suggests that the strange trip of Strongylus is just an evolutionary relic. Some day they may lose this heritage, but for now they still retain a vestige of their first go at parasitism, when bellies and mud stayed in close touch. On the other hand, some researchers think the parasites continue taking this journey because it benefits them. Parasitologists have compared species of nematodes such as Strongylus that wander through tissue with species that stay put in the intestines, and they’ve found a pretty consistent difference: the wanderers actually grow faster and end up bigger and more fertile. A trip through muscle means a respite from the gastric acid of the intestines, the slosh of digested food, the low oxygen levels, and the vicious blasts of the intestine’s powerful immune system. The trip may be a relic, but it’s a useful one.
The puzzle of parasite evolution gets even more confusing when you consider the things that happen to hosts when they are invaded by parasites. Filarial worms, which cause elephantiasis, enter the lymphatic system and start producing thousands of baby worms. Sometimes a person’s immune system reacts violently to the worms, scarring the lymph channels and blocking them up. The lymphatic fluid builds up in the lymph channels, producing elephantiasis—monstrously swollen legs, breasts, or scrotums. There’d be no sense in calling a swollen leg an adaptation of the parasite, since it does no good for the worm. It’s simply the immune system misfiring. It is nothing more than what Richard Dawkins has called a “boring by-product.”
The best way to tell whether a given change to a host is a boring by-product or a true adaptation is to study its evolution. One elegant test of this has been done with insects that make galls on plants. You may sometimes notice cherry-shaped balls hanging from the leaves of oak trees, or a flower’s stem bulging as if it had somehow swallowed a marble. These are galls: bits of plant tissue that have formed into shelters for insect parasites. Hundreds of different insect species live in galls, which can form on flowers, twigs, stems, or leaves. Some species of wasps, for example, lay their eggs on oak leaves, and the cells of the leaf respond to the egg by growing up and around it. The larva is born and becomes buried even deeper in the leaf. The cells multiply into a huge spherical shape, with an inner layer of hairy tissue. Food—starches and sugars, fats and proteins—is pumped into the gall from elsewhere in the plant and fills up the oversized cells in the inner hairs. The wasp larva bursts them open and feeds on the fluid cocktail. As it destroys the inner cells the outer ones divide and become ready to be eaten.
The galls are formed by the plants themselves, not the insects. Are they, as some researchers have suggested, just scars that happen to give the parasites some shelter? Warren Abrahamson of Bucknell University and Arthur Weis of the University of California at Irvine have performed some of the closest studies of galls, focusing on the goldenrod gallflies. The flies lay their eggs in a bud of a goldenrod plant in late spring. A spherical gall forms, growing to half an inch to an inch in diameter, and the fly larva grows inside. Parasitic wasps attack the fly larva, as do beetles. Woodpeckers and black-capped chickadees chip the galls open during the winter to eat them like some kind of delicious hard-shelled nut.
The galls in which these flies live vary in size and shape. Say for the moment that the galls are merely the boring by-product of a fly living within a goldenrod plant. Then you’d expect that any change in their variation from one generation to the next should be linked to changes in the genes plants use to defend themselves against invaders. Abrahamson and Weis have run experiments in which they raised gallflies on goldenrod plants that were all clones. Since their genes were identical, the plant’s defense against the flies should have been identical. Yet, Abrahamson and Weis found that the plants produced very different sorts of galls. That suggests that the flies’ genes are responsible for shaping the galls by taking control of the plant’s own genes. There’s probably some fierce natural selection going on in the flies for these genes, given that 60 to 100 percent of the galls are attacked by parasites. Supporting this, when the biologists observed the gallflies from generation to generation, a given lineage of flies all produced similar galls. The gall is made by the plant and yet is the work of the parasite, shaped by its evolution, not that of its host.
It’s actually surprising just how many things parasites do to their hosts that are not boring by-products but adaptations produced by evolution. Even harm itself is often an adaptation. Closely related parasites can be gentle or brutal to their hosts, or any shade in between. Leishmania can cause a few sores or eat away your face, depending on the species. Until recently, scientists didn’t think about how parasites could have such different effects on their hosts. The doctors were too busy looking for cures, and the evolutionary biologists were more interested in hosts than in parasites. They waved off the differences with a notion that when parasites first hop to a new host species they do a lot of damage. Once they’ve had a chance to fine-tune themselves, the story went, the parasites gradually mellow.
That’s certainly the case when many parasites accidentally find themselves in new hosts. A disease called sparganosis, for example, is caused by a species of tapeworm that uses copepods as its intermediate host and matures inside a frog. If a human should accidentally swallow the copepod in a glass of water, the tapeworm will escape out of the intestines and wander in confusion around the body, with none of the cues and landmarks it uses in a frog. As it zigzags randomly under the skin the tapeworm grows a few inches long, destroying tissue in its wake and inflaming its host into agony. If enough frog tapeworms found themselves inside humans, they might evolve into a new species better adapted to a new host. If they did, the conventional wisdom went, they would be amply rewarded by natural selection for any mutation that caused less harm to their new host. After all, if their host died off, the parasites would die with it. The wisdom of maturity brings gentleness.
It took until the 1990s for biologists to run the first experiments that could actually test this notion. A German evolutionary biologist named Dieter Ebert performed one of them, using water fleas. Water fleas sometimes suffer from a parasitic protozoan called Leistophora intestinalis, which lives in their gut and gives them diarrhea; the diarrhea carries the parasite’s spores with it, spreading them to other water fleas in the same pond. Ebert gathered fleas from England, Germany, and Russia and raised parasite-free colonies of each population. He then infected the colonies with Leistophora but used only the ones that had lived in the English ponds.
According to the conventional ideas about parasites, the English water fleas should have fared best. After all, the English Leistophora had spent untold generations inside the English water fleas and theoretically had come to a mellow coexistence. But Ebert found in fact that the opposite happened. The English fleas became burdened with many more parasites than the German and Russian fleas: they grew more slowly, they laid fewer eggs, and they died in greater numbers. Even though the English parasites had had more time to adapt themselves to English fleas, they had remained vicious.