Parasite Rex

6 Evolution from Within

The Origin of Species is a mournful book. God did not put species here on Earth balanced in perfect harmony, Darwin was saying. They are born out of a vast, ongoing death. “We behold the face of nature bright with gladness, we often see superabundance of food,” he wrote. “We do not see, or we forget, that the birds which are idly singing round us mostly live on insects or seeds, and are thus constantly destroying life; or we forget how largely these songsters, or their eggs, or their nestlings, are destroyed by birds and beasts of prey.” Most plants and animals never get a chance to reproduce, he argued, because they are killed by some predator or grazer, are outcompeted by members of their own species for sunlight or water, or just starve to death. The few that survive all these menaces and reproduce pass on their secret to success to the next generation. And out of all this death comes natural selection, which can transform it into the songs of birds, the leap of a flying fish—into a world that looks, at least on its surface, bright with gladness.

Yet, Darwin said little about one particularly powerful evolutionary menace, one that brought him a lot of personal sadness. His ten children struggled against diseases such as influenza, typhoid, and scarlet fever, and by the time The Origin of Species came out in 1859, three of them had died. Darwin himself suffered for much of his adult life with fatigue, dizzy spells, vomiting, and heart trouble. He once described his health this way: “Good, when young, bad for the past 33 years.” Although no one is sure what made him suffer, some have suggested that he had Chagas disease. Chagas disease is caused by Trypanosoma cruzi, a species of trypanosomes related to Trypanosoma brucei, the cause of sleeping sickness. T. cruzi slowly wrecks parts of the nervous system, and the ways to die of Chagas are horrible in their variety: your misfiring heart may stop beating, for example, or your intestines may stop getting the proper commands for peristalsis and let food pile up in the colon until you die of blood poisoning. T. cruzi is spread by the benchuca, a biting insect of South America, and Darwin was bitten by one as he was traveling the world on the H.M.S. Beagle; many of his symptoms arose only when he returned to England. The Darwins didn’t have to worry about getting eaten by wolves or starving to death, but infectious diseases—in other words, parasites—could still ravage them.

The toll that parasites take on the rest of life is far heavier—a toll that in terms of evolution is on par with predators and starvation. Viruses and bacteria tend to do their work quickly, multiplying madly and causing diseases that either kill or are defeated by the immune system. Eukaryotic parasites can be swiftly fatal as well—witness the brutality of sleeping sickness and malaria—but they can also do other kinds of damage. Ticks and lice may only live on the skin, but they can leave their host gaunt and emaciated. Intestinal worms can let their hosts live for years, but they stunt their growth and cut down their litters. The flukes that Kevin Lafferty studied in the Carpinteria salt marsh don’t destroy their killifish hosts themselves, but they turn them into dancing bird food. A crab infected with Sacculina may live a long life, but because it has been castrated by its parasite, it cannot pass on its genes. Evolutionarily speaking, it’s a walking corpse.

By keeping their hosts from passing on their genes, parasites create an intense natural selection. Perhaps parasites caused Darwin too much misery for him to recognize that they can be a creative evolutionary force in their hosts. A lot of the evolution that results takes place where you’d expect it: in the immune system, which defends animals from invaders. But it also brings out things that seem at first to have nothing to do with diseases. There’s growing evidence that parasites are responsible for the fact that we, and many other animals, have sex. The tail of a peacock, and other devices that males use to attract females, may be brought to us thanks to parasites. Parasites may have shaped societies of animals ranging from ants to monkeys.

Parasites have probably been driving the evolution of their hosts since the dawn of life itself. Four billion years ago, when genes formed loose confederations, parasitic genes could take advantage of them and get themselves replicated faster than the rest. In response, these early organisms probably evolved ways to police their genes. This sort of monitoring still goes on today in our own cells, which carry genes that do nothing but search for genetic parasites and try to suppress them.

When multicellular organisms evolved, they became a particularly choice target for parasites, since each one offered a big, stable habitat rich with food. And multicellular organisms had to fight a new sort of parasitism as well, in which some of their own cells tried to replicate at the expense of the rest of the organism (a problem we still face with cancer). All these pressures led to the evolution of the first immune systems. But for every step that a host takes against parasites, parasites are at liberty to evolve a step in response. Say an immune system evolves a tag it can put on parasites to make them more recognizable and easier to kill. The parasite can then evolve the tools it needs to rip that tag off. Immune systems became increasingly sophisticated in response; about 500 million years ago, for example, vertebrates evolved the ability to recognize specific kinds of parasites with T and B cells, and make antibodies to them.

This evolutionary back-and-forth didn’t just happen back in the depths of time. It happens today, and biologists can watch it in action if they run the right sort of experiment. A. R. Kraaijeveld of the Imperial College in England performed one such experiment with fruit flies and the wasps that parasitize them. For his experiment, he chose a wasp and two of its host species: the fruit flies Drosophila subobscura and Drosophila melanogaster. He raised the wasps on D. subobscura flies, and then put a few dozen of the parasites in a chamber with D. melanogaster. The wasps parasitized these new hosts, and they killed nineteen out of every twenty D. melanogaster. But one out of twenty D. melanogaster managed to marshal its immune system and kill the wasp larvae. Kraaijeveld took these resistant fruit flies and used them to breed the next generation of D. melanogaster.

Meanwhile, Kraaijeveld continued to raise his wasps on the other flies, D. subobscura. When the next generation of D. melanogaster had matured, he took some of the wasps and transferred them to their chamber. The wasps would then attack the new generation of D. melanogaster, and once again, Kraaijeveld would raise the survivors to produce a new generation.

By raising the wasps and the flies in this way, Kraaijeveld was blindfolding one of the boxers in his host-parasite match. With each generation, the D. melanogaster flies were able to adapt more and more to the wasps. But the wasps, which Kraaijeveld raised on another species of fly, didn’t have any chance to match the evolution of their D. melanogaster host. The mismatch let D. melanogaster steadily improve their fight against their parasites. In only five generations, the proportion of flies that could kill the wasp larvae rose from one in twenty to twelve in twenty.

Hosts and parasites may evolve together in a continual escalation (what biologists call an arms race), but in many cases their evolution can look more like a merry-go-round. Parasites evolve over time to do a better and better job of recognizing their hosts, finding weakness in their defenses, and thriving inside them. But a host species is never genetically uniform—it instead comes in strains, each with its own set of genes. Parasites have variations of their own, and some of them may help parasites against particular strains of hosts. Over time strains of parasites emerge, each adapted against strains of hosts.

Biologists have built mathematical models of these intimate relationships. If one strain of host is more common than the rest (call it Host A), any parasites that are adapted to it will have a rosy future. After all, they can hop between a wealth of hosts, replicating along the way. The problem is that, as parasites, they will kill or disable a lot of their hosts. From generation to generation, Host A will fade as its parasites undermine their success.

The attention that parasites pay to the most common host gives rarer host strains an advantage. Since the most common parasites aren’t adapted to attack them, they get the opportunity to multiply. As Host A declines, another host, say Host B, rises. But then parasites that can adapt to Host B get rewarded by natural selection and multiply as well. They eventually drive down Host B’s numbers, letting Host C ascend, then D, and E, and so on, maybe even back to Host A again. Every now and then a mutation creates a rare new strain of host. It simply becomes Host F and falls into the rotation.

This endless rise and fall would probably have appalled the biologists of Lankester’s day. They saw the history of life as a march of progress, always threatened by degeneration. In this new kind of evolution there is no progress forward or backward. Parasites force their host to go through a huge amount of change without going anywhere in particular. One variant rises, then it falls, and another variant rises to take its place, only to fall in turn. This sort of evolution isn’t the stuff of epic poetry but of surreal children’s stories. Biologists came to call it the Red Queen hypothesis, referring to the character in Lewis Carroll’s Through the Looking Glass who took Alice on a long run that actually went nowhere. “Now, here, you see, it takes all the running you can do, to keep in the same place,” the Red Queen declared.

Yet, there’s a paradox to the Red Queen hypothesis. While it’s all about running to stay in place, it may have allowed evolution to take one crucial step forward: it may have brought about the invention of sex.

In the early 1980s, Curtis Lively found himself in New Zealand wondering about sex. He had just finished earning a Ph.D. in evolutionary biology by studying the barnacles of the Gulf of California. One of the questions he had to answer on his qualifying exams was, Why did evolutionary theory have such a hard time accounting for sex? He had no idea.

It’s not a question that most people are accustomed to asking. “If you go into a class of sophomores and ask, ‘Why are there males?,’ they look at you as if you’re crazy,” Lively says. “They’ll say you need males to reproduce and that each generation produces more males. Well, that may be true for mammals, but for many species that’s not true. It’s just staggering to them to think that anything could do that, could reproduce without males and sex. Sex and reproduction are just fused in most people’s brains.”

Bacteria simply divide themselves in two when the time seems right, as can many single-celled eukaryotes. Many plants and animals have the ability to reproduce themselves on their own quite comfortably. Even among the species that do reproduce sexually, many can switch over to cloning. If you walk through a stand of hundreds of quaking aspen trees on a Colorado mountainside, you may be walking through a forest of clones, produced not by seeds but by the roots of a single tree that come back up out of the ground to form new saplings. Hermaphrodites, such as sea slugs and earthworms, are equipped with male and female sex organs and can fertilize themselves or mate with another. Some species of lizards are all mothers: in a process called parthenogenesis, they somehow trigger their unfertilized eggs to start developing. Compared with these other ways to reproduce, sex is slow and costly. A hundred parthenogenetic female lizards can produce far more offspring than fifty males and fifty females. In only fifty generations, a single cloning lizard could swamp the descendants of a million sexual ones.

When Lively was learning about the mystery of sex, there were only a handful of good hypotheses to explain why it existed at all. Two of the favorites were nicknamed the Lottery and the Tangled Bank. According to the Lottery hypothesis, sex helped life survive in unstable environments. A line of clones might do well enough in a forest, but what if that forest changed over a few centuries to a prairie? Sex brought the variations that could allow organisms to survive change.

According to the Tangled Bank hypothesis, on the other hand, sex gets offspring ready for a complicated world. In any environment—a tidal flat, a forest canopy, a deep-sea hydrothermal vent—the space is divided into different niches where different skills are needed for survival. A clone specialized for one niche can give birth only to offspring that can also handle the same niche. But sex shuffles the genetic deck and deals the offspring different hands. “It’s basically spreading out progeny so that they’re using different resources,” says Lively. The progeny wouldn’t have to fight with each other over food as much, and thus a mother would be more likely to become a grandmother. While the Tangled Bank hypothesis might work in theory, it wasn’t very likely. The different kinds of bodies built by the different sets of genes had to be quite distinct from each other in order for it to work. Nevertheless, it was the dominant idea at the time.

Lively found himself in New Zealand in 1985 because his wife, Lynda Delph, wanted to study evolutionary biology at the University of Canterbury. Lively got a job there as a postdoctoral researcher, and he wondered if New Zealand might offer him a way to test the different explanations for sex. In evolutionary biology, ideas tend to bubble up fast and easily, and often turn out to be miserably untestable. To test explanations for sex, Lively would have to find the right species to study. It would have to be a mix of sexuals and asexuals. Among some animal species, for instance, there are populations of males and females that live alongside clones. Other species are hermaphrodites, and they can choose to have sex with themselves or with another animal. Only in these sorts of animals could the generation-by-generation effects of evolution be seen, because a biologist could compare how the sexuals and asexuals fared. “If you’re dealing with something that’s all sexual,” says Lively, “it’s hard to know what selection would be for or against an asexual. But if you have a system where you have both, now you have the basis for comparison.” He couldn’t test an idea about the persistence of sex in humans, for instance, because we all do it. There is no lost tribe out there who can have children with natural cloning. In our own evolutionary lineage, the race between the sexuals and the asexuals ended hundreds of millions of years ago.

As luck would have it, there was a snail in New Zealand that fit Lively’s research perfectly. Named Potamopyrgus antipodarum, the quarter-inch snail lived in most lakes, rivers, and streams in the country. While most populations of the snail were all identical clones, the product of parthenogenesis, some were divided into male and female forms that used sex to reproduce.

Lively set out to see if the habitats of the snails had any influence on how they reproduced. The snails that lived in the streams faced sudden floods, while the ones that lived in lakes enjoyed a peaceful, stable existence. According to the Lottery hypothesis, the snails in the streams should favor sex because they had to survive in an unstable place. According to the Tangled Bank hypothesis, there would be more competition in the lakes for different niches, and the males would be in demand there.

Lively hiked to the high mountain lakes where the snails lived and waded into the waters with his net. He gathered the snails there, and to determine their sex, he cracked open their shells and cut them open, looking for a penis behind their right tentacle. But when he looked inside the snails, he was baffled—they were packed with what looked to him like giant sperm. “I showed them—unfortunately for me—to one of the parasitologists at the university, and he said, ‘They’re not sperm, you idiot, they’re worms.’” The parasitologist explained to Lively that the parasites were flukes that castrated their snail hosts, multiplied, and eventually got into their final host, a duck. In some places, the parasitologist told him, the snails were riddled with the flukes, and in others they were free of them.

The humiliation wasn’t hard to handle, though, because Lively realized that these parasites might let him test a third explanation for the endurance of sex: that parasites were responsible. The idea had been offered up in various forms by various scientists, but most fully in 1980 by an Oxford University biologist named William Hamilton. Hamilton argued that when hosts are faced with the Red Queen, sex can be a better strategy for fighting parasites than cloning.

Consider a bunch of amoebae that reproduce by cloning and that are divided up into ten genetically distinct strains. Let’s say that bacteria infect them and the Red Queen’s race begins. The bacteria come in strains of their own, each adapted to a different strain of host. The most common strain of amoebae are pounded down by their strain of bacteria, and when that strain of amoeba loses enough numbers, the parasitic spotlight switches to a different strain. Because these amoebae clone to reproduce themselves, every new generation of amoebae will be genetically identical with their forebears. The bacteria sweep through the same ten strains over and over again, and after a while, they may drive some of those strains into extinction.

Now imagine that some of these amoebae evolve the means to have sex. The males and females make copies of their genes and join them together to form their offspring’s DNA, and as the genes combine, they get shuffled around. As a result, the offspring isn’t a carbon copy of one of its parents but a new jumble of tier genes. Now the parasites have a much harder time chasing their hosts. Because the genes of the sexual amoebae mix, they no longer come in distinct strains, and it becomes harder for parasites to get a lock on them. The Red Queen still takes sexual organisms for an endless run, but their offspring may have less of a chance of getting infected. And the protection that this diversity brings to the sexual amoebae might give them a crucial edge in their competition with asexuals.

It was an elegant idea, but Lively didn’t actually believe it when he first read about it. “My feeling—and I think it was general—was that it was a very clever idea, but it seemed unlikely to me to be true. The reason is that I just didn’t see much parasitism in the world. If you’re going to have a selective pressure that’s intense enough, it should be something that has big, immediately obvious effects. At least in humans in this country, we don’t see those big effects. And the people doing field biology were mainly interested in competition or predation. There was no tradition in parasites.”

But the fact was that most animals—Lively’s snails included—are rife with parasites. On the outside chance Hamilton might be right, Lively decided to start noting whether or not his snails were infested with the flukes. “The theory for parasites was just being laid by Hamilton in 1980, 1981, 1982, but no one had discovered systems where you could test them. I didn’t know I was dealing with one until I started cracking open these snails. I realized it would be able to address Hamilton’s idea, but if they had been viruses I would not have known it. Here we’re dealing with big honking swimming worms, and anyone can see them under a dissecting microscope.”

It didn’t take Lively long to see a clear pattern. The snails in the lakes were more infected with the flukes than the ones in the streams, and it was in the lakes that there were the most males. The more infested a given lake was, the more males it held. The only hypothesis that could account for all three patterns was the Red Queen: in places where there were more parasites, there was a stronger evolutionary pressure for sex. “I was completely surprised. When I had half the data set I eventually published, I thought, ‘Wow, there’s a trend setting up.’ So I went out and got a lot more data to see if it went away. It didn’t. Adding more lakes didn’t change it—it wasn’t a few lakes that were highly sexual and highly infected.”

Lively published those first results from New Zealand snails in 1987. He has made the study of sex his preoccupation ever since. He’s tested the Red Queen hypothesis in other ways and found more support for it. In 1994, for example, he traveled to Lake Alexandrina on the southern island of New Zealand with his postdoctoral student Jukka Jokela. They gathered snails from both shallow and deep waters. In the shallow waters the snails live alongside ducks, which are the final hosts for the flukes, and the ducks shed the flukes’ eggs there. With so many eggs in the water, the snails are sicker in the shallows than farther from the shore. Lively and Jokela found that there are more males among the snails in shallow water as well, probably as a result of the pressure of parasites. In a single lake, they could see parasites shaping the sex lives of their hosts.

At the same time, Lively has watched other biologists find the Red Queen at work in other species. In Nigeria there lives another snail named Bulinus truncatus, one of the species that carry the blood flukes that cause schistosomiasis. Its sex life is more exotic than that of Lively’s New Zealand snails. Every one is a hermaphrodite, with male and female gonads it can use to fertilize its own eggs and produce clones. But some of them also come equipped with a penis, which they can use to mate with other snails.

As with the New Zealand snails, it seems like a huge waste of effort for the Nigerian species to grow a penis and have sex when it can just fertilize itself. And as in New Zealand, parasites seem to make the effort worthwhile. According to the parasitologist Stephanie Schrag, each year the snails have a penis season. The waters are coolest in northern Nigeria in December and January. The snails use the cool temperature as a cue to produce more offspring equipped with penises—snails, in other words, that can mate with other snails. With more penises, there’s more sex among the snails, and more shuffling of their DNA, and more variation in the next generation. The snails need about three months to mature, so this new sexually produced generation comes of age between March and June. And March to June happens to be the time of year when flukes are at their worst in northern Nigeria. In other words, snails seem to use sex to prepare months in advance for an annual attack of parasites.

The most unexpected support for the Red Queen’s effect on sex has come from parasites themselves. Like their hosts, many parasites have sex, and in 1997, Scottish scientists asked why parasites bother. Like Lively, they looked for a species that isn’t stuck reproducing only sexually or asexually. They chose Strongyloides ratti, a nematode that, as its name suggests, lives inside rats. The females living in the guts of rats lay eggs without any help from males. Once these eggs leave the rat’s body they hatch, and their larvae emerge as one of two different forms.

One form is all female, and it spends its time looking for a rat to penetrate. It gets into the skin of the rat and then glides through it until it reaches the rat’s nose. There it finds the nerve endings that the rat uses to smell, and it follows them into the brain. From there the parasite takes a route—no one knows the details—all the way to the rat’s intestines, and starts making female clones again.

The other form of the nematode hatches from eggs in the soil and stays there. When the larvae mature, they turn into both females and males rather than females only, and instead of cloning they have sex to reproduce. The females lay fertilized eggs, giving birth to a new generation of worms that can penetrate the skin of rats and get back into their gut. In other words, Strongyloides can complete its life cycle with sex or without.

The Scottish scientists decided to see whether a change in the immune system of a rat might influence the kind of reproduction the parasites chose. They put Strongyloides into rats, and the rats mounted an immune response to the parasites. They then gave the rats shots of antiworm medicine to clear the parasites out of their bodies. Now the rats were primed to fight off a second invasion. When the scientists reinfected the rats and the new wave of nematodes began making eggs, the parasites that emerged from them were more likely to be sexual forms. In another experiment, the scientists depressed the immune system of a rat with radiation and then infected it with Strongyloides. They found that the parasites were much more likely to clone themselves than to have sex.

These experiments showed that Strongyloides would prefer to reproduce asexually, but a healthy immune system forces it to have sex. “Your immune system is a sort of parasite of the parasite,” says Lively. Like parasites, T cells and B cells multiply into many different lineages, and the most successful killers get to reproduce themselves the most. Like their hosts, parasites can defend themselves by having sex and diversifying their genes.

All the work that Lively and these other scientists have done on the origins of sex rests on the Red Queen’s shoulders, and yet it has been hard to get a glimpse of the Queen herself. Some researchers who run computer simulations of the struggle between host and parasite have seen her shadow flit across their monitors. In Lively’s own work, he could see her effects only by mapping where the sexual and asexual snails lived—taking a snapshot of her effects at a given instant. But eventually he had studied enough snails to see her work spread across time rather than space.

For five years he and another of his postdoctoral students; Mark Dybdahl, netted snails in Lake Poerua. The snails there were all clones, and most of them belonged to four main lineages. Lively and Dybdahl took a census of the four snail clans each year and watched their populations rise and fall. They took the rarest clones and the common ones to their lab at Indiana University, where Lively now works. There they exposed both kinds of snails to their flukes. They found a huge difference: the parasites had a much harder time infecting the rare snails than the common snails. Here was a central prediction of the Red Queen: that being rare gives an organism an advantage, because parasites are more adapted to the more common hosts.

They then looked at their census of the snails of Lake Poerua over five years. In a given year, they found, there wasn’t much of a connection between the number of parasites infecting a lineage of snails and how big the lineage was. The ones with heavy burdens of parasites weren’t the most common. But with a five-year record, Lively and Dybdahl could look back at the lineages in previous years. When they did, a distinct pattern jumped out. The snail lineages that carried the heaviest burdens of parasites in a given year had been the most common snails a few years before, and now they were declining. The snails had started out rare and had increased their numbers, but eventually the parasites caught up with them and started driving their numbers down. Because it took a while for the evolution of the flukes to catch up with their hosts, the flukes reached their greatest success only after the snails had already started to decline.

For the first time, scientists have been able to see the Red Queen at work, by moving back through time. It’s a method that Alice would have approved of. At one point in her adventures, she lost sight of the Red Queen. She asked the Rose how to catch her, and the Rose replied, “I should advise you to walk the other way.”

“This sounded like nonsense to Alice, but after only occasional glimpses of the Queen in the distance, she thought she would try the plan, this time, of walking in the opposite direction. It succeeded beautifully. She had not been walking a minute before she found herself face to face with the Red Queen.”

Shortly after William Hamilton proposed that parasites drive the evolution of sex, he realized that this idea naturally gave rise to another one. Sex may help organisms fend off parasites, but it brings trouble of its own. Say you’re a hen, and your genes are particularly well suited to fighting off the parasites that the Red Queen has made most common at the moment. You want to have some chicks, but to do that you have to find a rooster, and half of the chicks’ genes will have to come from him. If you pick a rooster that has bad parasite-fighting genes, your chicks will suffer the consquences. It pays for you to be picky about your mates and to try to figure out which roosters have good genes. The rooster doesn’t have to be as picky, because he can make millions of sperm. You, on the other hand, can raise only a few dozen eggs over your lifetime.

Working with a graduate student, Marlene Zuk, at the University of Michigan, Hamilton suggested that females judge male displays to decide how well they can fight parasites. A weak suitor will have to spend most of his efforts fighting off parasites and will have very little resources left over. But a male who can resist parasites will still have enough energy left over to advertise his healthy genes to females. These advertisements, Hamilton and Zuk argued, should be showy, extravagant, and expensive. A rooster’s comb might qualify as just this sort of biological resumé. It serves no particular purpose in the rooster’s survival. In fact, it’s a burden to him, because in order to keep it red and puffy, the rooster has to pump testosterone into it. Testosterone tends to depress the immune system, putting roosters at a disadvantage in fighting off parasites.

Just as parasites might create the rooster’s comb, they might draw out the long tail feathers on birds of paradise. They might make redwing blackbirds redder, they might put bright spots on male stickleback fish, and they might make the sperm packages of crickets bigger. Anything that females could use to judge males might be influenced by parasites.

Hamilton and Zuk presented their idea in the early 1980s, with a simple test. You’d expect that on the whole, the members of a species saddled by many parasites would be showier than a species with a lighter load. According to their hypothesis, bacteria and viruses wouldn’t have a big impact on male display. They tend to kill their hosts or get killed by them. In the first case, there’s no male left to do the displaying; in the second, a sick male could recover so well he’d be indistinguishable from stronger males.

Hamilton and Zuk gathered reports on North American songbirds and their parasites that cause chronic, grinding diseases—bird malaria, for example, and Toxoplasma, trypanosomes, and various worms and flukes. They then rated the showiness of the males of each species in terms of their brightness and their song, and found that the species with the most parasites had the strongest male displays.

That initial work inspired a huge amount of research (more, actually, than Hamilton’s broader theory on the origin of sex itself). Zoologists tested these ideas in the songs of crickets, in the spots on stickleback fish, in the throat pouches of fence lizards. In many of the tests—especially the lab experiments—Hamilton and Zuk fared well. Zuk studied red jungle fowl from Southeast Asia, for example, which are wild relatives of chickens. She kept track of the choices made by female jungle fowl in her lab and measured the combs on the males they chose. Females, she found, consistently preferred males with longer combs.

In a more elaborate study, Swedish scientists studied wild ring-necked pheasants. Male pheasants have spurs on their legs, and the researchers found that the females used the length of the spur to decide which male to mate with. The researchers then looked at the immune system genes of the pheasants and found that the pheasants with the longest spurs shared a particular combination of genes. They don’t know what those genes actually do to help the males fight off parasites. But they observed the offspring of the pheasants and found that the ones with long-spurred fathers had better chances of surviving than those with short-spurred ones.

There’s no reason why these antiparasite advertisements can’t extend beyond a male’s body to the way he courts females. That certainly seems to be what’s going on with the fish Copadichromis eucinostomus, which lives in Lake Malawi in central Africa. To attract females, the males build bowers out of sand on the lake bottom. Some of them are nothing more than a handful of grains sitting on top of boulders, while others are big cones several inches high. The males build their bowers together, creating dense neighborhoods, and each defends his own against roaming males that are trying to usurp him. The female fish spend most of their time feeding on their own, but when the time comes to mate, they go to the bower neighborhood and inspect the males’ work. If a female chooses to mate with a male, she releases an egg and puts it in her mouth. The male puts his sperm in her mouth and she carries away the fertilized egg.

The females apparently use the bowers to find out which males do the best job of fighting parasites such as tapeworms. Experiments have shown that the females prefer males who built big, smoothly shaped bowers, and these males also happen to be the ones who carry the fewest tapeworms. A fish that’s carrying tapeworms may have to spend so much time eating that it can’t maintain its bower. The bower thus becomes a medical chart, and perhaps a genetic profile.

But the Hamilton-Zuk hypothesis has failed several tests as well. Male desert toads attract their mates with their calls, for example, but a loud call doesn’t reflect an immune system better able to fight off Pseudodiplorchis, the parasite that lives in their bladder and drinks their blood. In some species of fence lizards, the males have brightly colored throat flaps that females just adore, but there’s no connection between their brightness and parasites such as Plasmodium that attack the lizards.

These failures have made scientists wonder whether they’ve been testing the Hamilton-Zuk hypothesis the wrong way. A particular parasite may be harmful or harmless, and may therefore have a big influence on a male’s display or none at all. If you have a lot of studies on the loads of different parasites, it’s hard to use them to come up with any sort of general conclusion. Rather than counting the parasites themselves, measuring the immune system may be more reliable. Immune systems have evolved to cope with many different kinds of parasites, so they can offer a better overall clue. It’s a lot harder to count microscopic white blood cells than giant tapeworms, but it turns out to be a better method. Immune studies give the Hamilton-Zuk hypothesis strong, consistent support. Peahens, for example, choose peacocks with more extravagant tails, and researchers have found that peacocks with more extravagant tails have immune systems that can mount a stronger response to parasites.

Another reason why the Hamilton-Zuk hypothesis is falling short may be that scientists are looking at the wrong signals. They’ve stuck with visible cues like rooster combs and lizard pouches because they’re easy to measure. But among the channels of communication between the sexes, vision may not be all that important. Mice, for example, can smell the urine of a prospective mate and tell whether or not it’s carrying parasites; if a male mouse is sick, a female will stay away. It’s even possible that males could use their odors to advertise their strength against parasites with some kind of extravagant, irresistible perfume. “The scent of a male mouse,” writes one biologist, “is the chemical equivalent of a peacock’s plumage.”

And even if Hamilton and Zuk’s idea turns out to fail for other animals, parasites may well have shaped their sex lives anyway for very different reasons. Once again, it all comes down to how a given animal passes on its genes. Among bees, young queens leave their birthplace hive at the end of the summer with a retinue of males. After she mates with them, the males then die, but the queen survives the winter and emerges in the spring to start a new colony with the eggs that were fertilized the previous fall. Every species of bees, in other words, flows through the bottleneck of its few queens.

By studying the DNA of bees, biologists have found that the queens may mate with ten or twenty males during their nuptial flight. That much sex, pleasure aside, is costly: a mating queen is more vulnerable to a predator’s attack, and she could save the energy involved in all that sex to survive the winter.

Bees may be having all that sex as a defense against parasites, as demonstrated by Paul Schmid-Hempel, a Swiss biologist. He injected sperm into queens and then raised the colonies the queens gave birth to. Some queens got the sperm of only a few closely related males, while others got a cocktail with four times more genetic diversity. When the queen’s colony began to hatch, Schmid-Hempel put the colonies out in a flowering meadow near Basel and left them there until the end of the season, when he went out to capture them.

By just about every measure, the offspring of high-diversity queens were far stronger against parasites than were the low-diversity ones. Their colonies had many fewer infections, fewer kinds of parasites invading, and fewer parasites in a given individual. The offspring of high-diversity queens were more likely to survive till the end of the summer, which made it more likely that they’d produce future colonies. Instead of carefully eyeing up a single male to mate, a queen bee may look for many suitors to create a genetic rainbow in her future hive.

As critical as an immune system may be to surviving parasites—particularly an immune system that can evolve rapidly—it’s really a defense of last resort. It fights against invaders that have already crossed the moat and are inside the castle. It would be far better to keep the parasites from getting in at all. Evolution has obliged. Hosts have adapted to fight off parasites with the shapes of their bodies, their behavior, the way they mate, even the shape of their societies—all designed to keep parasites at a distance.

Many insects are shaped expressly to fend off parasites. During their larval youth, some species are covered in spikes and tough coats that discourage wasps from trying to lay their eggs inside. Some have tufts of detachable barbs on their bodies, which entangle a wasp when it tries to land on them. When butterflies form cocoons, they sometimes dangle them from a long thread of silk that makes it impossible for wasps to get enough leverage to stab through their coat.

For some insects, armor is not enough. Thousands of species of ants, for example, are tormented by thousands of corresponding species of parasitic flies. The fly perches above the trail made by the ants from their nest to their food. When a suitable ant passes underneath, the fly dives down onto the ant’s back and wedges its egg-laying tube into the chink between the ant’s head and the rest of its body. Quickly the eggs hatch, and the maggots chew their way into the ant’s interior and then travel to the ant’s head. These larvae are muscle eaters. In a mammal it might make sense for them to make their way into a bicep or a thigh, but in ants the fleshiest place is the head. Unlike our brain-crammed skulls, those of ants hold only a loose tangle of neurons, the rest of the space being dedicated to muscles that power its biting mandibles. A maggot inside an ant’s head chews on the muscles, carefully avoiding the nerves, and grows until it fills the entire space. Finally, one day, the ant meets its awful end: the parasite dissolves the connection between the head and the rest of the body. Like a ripe orange, it drops to the ground. While the headless host stumbles around, the fly begins its next stage, forming its pupa. Other insects have to weave their cocoons exposed to the elements and hungry predators, but the fly develops snug in the tough cradle of an ant’s head.

These flies are so destructive that ants have evolved defensive manuevers against them. Some will run to escape the flies; others stop in their tracks and begin flailing wildly, gnashing their mandibles as soon as they even sense that a fly is overhead. A single parasitic fly can stop a hundred ants in their tracks along six feet of their trail. If the fly lands on the back of one species and gets ready to lay its eggs behind the head, the ant suddenly snaps its head back against its body, crushing the fly in its vise.

Among the leaf-cutting ants, these flies have transformed their entire social structure. Leaf-cutting ants travel from their nests to trees, hack off foliage, and take it back home, forming a parade of green confetti on the forest floor. Leaf-cutters are the dominant herbivores in many forests of Latin America—wildebeest in miniature, although they don’t actually eat the leaves. Instead, they bring them home to their colonies, where they use them to grow gardens of fungi, which then become their meal. If you want to get technical, leaf-cutters aren’t so much herbivores as mushroom farmers.

Leaf-cutter colonies are divided into big ants, which carry the leaves home, and little ants. The little ants (known as minims) tend the gardens, and they can be also found riding atop the leaves being brought home by the big ants. Entomologists have puzzled for a long time over why the minims would waste their time hitching rides like this. Some suggested that they must collect some other kind of food on the trees, maybe sap, and then go home on the leaves in order to save energy. In fact, minims are parasite guards. The parasitic flies that attack leaf-cutters have a special approach to their hosts: they land on the leaf fragments and crawl down to where the ants grip it in their mandibles. The fly then lays eggs in the gap between the mandible and the ant’s head. The hitchhiking minims patrol the leaves or perch on top, their mandibles open. If they encounter a fly, they scare it away or even kill it.

For bigger animals, the struggle with parasites is just as intense, although it’s not as obvious as an ant wrestling a fly. Mammals are continually assaulted by parasites—by lice, fleas, ticks, botflies, screwworms, and warbleflies—that suck blood or lay their eggs in the skin. In response, mammals have evolved into obsessive groomers. The way a gazelle lazily flicks its tail and nuzzles its flank may look like the picture of peace, but it’s actually in a slow-motion struggle against an army of invaders. The gazelle’s teeth are shaped like rakes, not to help it eat but to scrape away lice and ticks and fleas. If its teeth are blocked, its load of ticks will explode eightfold. Gazelles don’t groom themselves in response to any particular scratch; they clean themselves according to a clocklike schedule because parasites are so relentless. Grooming cuts into the time an animal needs to eat and guard against attacks from predators. The top impala in a herd ends up riddled with ticks—six times more than females—because he is too busy staying vigilant against male challengers.

The shape of an animal’s society may also help cut down on parasites. Animals protect themselves from predators in this way. Fish that stay in schools can pool their vigilance; as soon as any of them senses a predator, they can all swim away. And even if the predator should attack, each member of the school has lower odds of being killed than if it were on its own. It’s time to put the parasite alongside the lion. Increasing the size of a herd not only will lower the odds that each gazelle will be eaten by a lion, but also will lower the odds that each individual will be attacked by a tick or some other blood-sucker. On the other hand, parasites may simultaneously keep herds from getting too big. As animals crowd together in bigger and bigger groups, they make it easier for some parasites to be passed from host to host, whether they are viruses carried on a sneeze, fleas passed on with a nuzzle, or Plasmodium carried by a hungry mosquito.

Parasites may even teach animals manners, according to Katherine Milton, a primatologist at the University of California at Berkeley. Milton studies the howler monkeys of Central America, and she’s been struck by the viciousness of one of their parasites: the primary screwworm. This fly searches for open wounds on mammals; it can even find the hole made by a tick bite. It lays its eggs inside the wound, and the larvae that hatch start devouring their host’s flesh. They do so much damage in the process that they can easily kill a howler monkey.

The screwworm may make howler monkeys leery of fighting with each other over mates or territory. The fight might only be a minor scuffle, but if a monkey gets a scratch, a screwworm could make it the last scuffle it ever has. Screwworms are so efficient at finding wounds, in fact, that evolution may frown on violent howler monkeys. Instead, it may have made them affable creatures, and it may have encouraged them to evolve ways to confront each other without getting hurt, such as howling and slapping rather than biting and scratching. There are many other mammals that also have ways to avoid fights, and it’s possible that they are also trying to avoid parasites.

The best strategy for a host is simply not to cross paths with a parasite at all. Some of the adaptations hosts make to avoid the notice of parasites are so grotesque, so outrageous, that it’s hard to tell at first that they actually are designed for parasites at all. Consider leaf-rolling caterpillars. They’re pretty ordinary insect larvae with one exception: they fire their droppings like howitzers. As a bit of frass starts to emerge from the caterpillar it pushes a hinged plate back against a ring of blood vessels surrounding its anus. The blood pressure builds up behind the plate, which the caterpillar then releases. The pressure of the blood slams against the droppings so suddenly that it blasts them three feet a second, in a soaring arc that carries them up to two feet away.

What on Earth could have driven the evolution of an anal cannon? Parasites could. When parasitic wasps home in on a larva such as the leaf-roller caterpillar, one of the best clues is the odor of their host’s droppings. Since caterpillars are sedentary, not racing from branch to branch, their droppings will normally accumulate close by them. The intense pressure put on leaf-roller caterpillars by wasps has pushed the evolution of high-pressure fecal firing. By getting their droppings away from them, the caterpillars have a better chance of not being found by wasps.

Vertebrates, like insects, will also go out of their way to avoid parasites. Cow manure fertilizes the grass around it, making it grow lush and tall, but the cows generally stay away. They keep their distance because the manure often carries the eggs of parasites such as lungworms, and the parasites that hatch from them crawl up the neighboring blades of grass in the hope of being eaten by a cow. Some researchers have suggested that mammals that make long migrations, such as caribou and wildebeest, plot their course in part to avoid parasite-thick spots along the way. Swallows will fly back to their old nests and reuse them, unless they discover that their nests have been infested with worms and fleas and other parasites, in which case they’ll build a new one. If baboons discover that the area where they sleep has been overrun with nematodes, they’ll go away and won’t return until the parasites have died away. Purple martins go so far as to line their nests with plants like wild carrot and fleabane that contain natural parasite-killers. Owls sometimes catch blind snakes, but rather than tear them apart to feed their chicks, they drop them into their nests. There the snakes act as maids, slinking into the nooks of the nest and eating the parasites they find there.

Even if your mother was an excellent judge of fish bowers, even if you perfected your fly-killing head-snap, even if you can blast your frass into the neighboring meadow, you may end up with a parasite inside you. Your immune system will do its level best to stave off the invasion; it’s an exquisitely precise system of defense brought about thanks to the evolutionary pressure of parasites. But hosts have evolved other kinds of warfare. They can enlist other species to help them; they can medicate themselves; they can even reprogram their unborn offspring to prepare for a parasite-ridden world.

When a plant is attacked by a parasite, it defends itself with its own version of an immune system by creating poisonous chemicals that the parasite eats as it chews on the plant. But it also fights by sending out cries for help. When a caterpillar bites a leaf, the plant can sense it—a feeling not carried by nerves but felt nevertheless. And in response, the plant makes a particular kind of molecule that wafts into the air. The odor is like perfume for parasitic wasps; as they fly around searching for a host they are powerfully lured by the plant’s smell. They follow it to the wounded leaf and find the caterpillar there, and they inject it with eggs. These conversations between plants and wasps are not only timely but precise. Somehow the plant can sense exactly which species of caterpillar is dining on it and spray the appropriate molecule into the air. A parasitic wasp will respond only if the plant lets it know that its own species of host sits on a leaf.

Animals will sometimes defend themselves against parasites with a change of diet. Some will just stop eating—if a sheep is hit by a bad dose of intestinal worms, for instance, it may graze only a third of its normal intake. Such a change clearly can’t benefit the parasite, which wants the sheep to eat a lot so that it can eat a lot and make a lot of eggs. Researchers suspect that eating less may somehow boost the host’s immune system, making it better able to fight the parasite. On the other hand, the animals may not be simply fasting but may be being choosier about what they eat, choosing food that has the right nutrients to help them fight the infection.

Sometimes animals under attack by parasites will start eating foods they almost never eat. Some species of woolly bears, for example, normally eat lupine. They sometimes get attacked by parasitic flies that lay eggs in their bodies. Unlike the flies that attack ants or other insects, though, these parasites don’t always kill their hosts when they emerge from their bodies. And the woolly bears improve their own odds of survival by switching from a diet of lupine to one of poison hemlock. The parasitic flies still crawl out of their bodies, but some chemical in the hemlock helps the woolly bears stay alive and grow to adulthood. The woolly bears, in other words, have evolved a simple kind of medicine. Medicine may be pretty widespread among animals—there are plenty of records of animals sometimes eating plants that can kill parasites or expel them out of their gut. But researchers are still trying to prove that they actually eat those foods when they get sick.

When things get truly bleak—when there’s little hope a host can kill a parasite inside it—it cuts its losses. It has to accept that its life is doomed. Evolution has given hosts ways to make the best of the time they have left. When some species of snails are infected with flukes, there’s only a month or so before the parasites castrate them and turn them into nothing more than food-gathering slaves. That still gives the snails a month to produce the last of their offspring. They take full advantage, producing a final burst of eggs. If a fluke gets into a snail that’s still sexually immature, it will respond by developing its gonads much faster than if it were healthy. If they’re lucky, the snails can squeeze out a few eggs before the parasites cut them off.

When the fruit flies of the Sonoran desert are attacked by parasites, their response is to get horny. They feed on the rotting flesh of the saguaro cactus, and sometimes they encounter mites there. The mites leap onto the flies and jab their needlelike mouths into their bodies, sucking out their internal fluids. The consequences can be grave—a heavy infestation of mites can kill a fly in a few days. Biologists have found a big difference between the sexual activities of healthy and mite-infested male fruit flies. The parasites trigger the males to spend more time courting females, and the more parasites a male has, the more time he spends doing so, in some cases tripling his efforts.

At first this might seem like another display of puppetmastery, as a parasite speeds up its own transmission by putting infected flies in contact with healthy ones. In fact, the mites seem to get on flies only when they feed on cactus. They never hop from one mate to another. It appears that parasites have essentially driven flies to evolve a habit of mating more when death—and no more matings—seems imminent.

Why don’t the flies make the fast-and-furious lovemaking style a permanent one? The answer, probably, is that the mites aren’t always assaulting the flies. Some cactuses are covered with them; others are mite-free. As with bees, sex puts a lot of demands on fruit flies, making them an easy target for predators. Better to be flexible, mating at a slower speed normally and speeding up in the face of parasites.

Lizards are also tormented by mites of their own; they can die from an infestation, and the survivors are likely to have their growth stunted. But when they’re attacked, they go through a different sort of change: they alter their unborn offspring. A lizard infested by mites produces babies that are bigger and faster than those born of healthy parents. A healthy baby lizard will have a growth spurt in its first year and then grow more slowly for the rest of its life. But a lizard born to mite-ridden parents will grow fast for its first two years or more. Lizard mothers apparently can program the growth of their offspring to adapt to the presence of parasites. If there are no mites around, their offspring can grow slowly and live a long life. But if mites turn up, it pays to grow faster in order to reach a healthy weight as an adult, even if that means dying sooner.

And if a host is doomed to die, it can do its best to spare its kin. Worker bumblebees spend their days flying from flower to flower, collecting nectar and bringing it back to their hive. At night they stay in the hive, kept warm by the heat of thousands of flapping wing muscles. On its travels for nectar, a bumblebee may be attacked by a parasitic fly, which lays an egg in its body. The parasite matures within the bumblebee, and in the warmth of a beehive its metabolism runs so quickly that it can finish growing up in only ten days. The fly emerges from its host and can infect the rest of the hive. Yet, many parasitic flies don’t get that luxury because their host does something strange: it starts spending its nights outside the hive. By staying out in the cold, the worker slows down the parasite’s development. It also prolongs its own life. The combined effect makes it unlikely that the parasite will ever make it to maturity before the bee itself dies. In this way, the bumblebee prevents an epidemic from breaking out in its hive.

As cunning as these kinds of counterattacks may be, parasites can evolve counter-counterattacks. If a cow avoids manure to keep away from the lungworms it holds, the parasites will leave the manure. When a lungworm drops to the ground in the manure, it bides its time until light strikes it. That is its signal to climb upward until it reaches the surface of the manure. It begins to hunt around for a species of fungus that is also a parasite of cows—a species that also responds to light by growing little spring-loaded packages of spores. As soon as the lungworm touches the spore package, it latches on and climbs up to the top. The fungus catapults itself six feet into the air and soars away from the manure. The lungworm rides it like a puddlejumper, and out of range of the manure it has better odds of being eaten by a cow.

Study arms races long enough, and you start to imagine that hosts and parasites could carry each other into the clouds, each driving the evolution of its counterpart so hard that they become all-powerful demigods hurling lightning bolts at each other. But of course the race has limits. When Kraaijveld set his wasps against his fruit flies, the fruit flies reached a 60 percent resistance to the wasps after only five generations, but in later generations the resistance simply stayed there at 60 percent. Why didn’t it keep rising to 100 percent, creating a race of perfectly immune flies? Fighting parasites comes at a high cost. It requires energy to make the necessary proteins—energy that can’t be channeled somewhere else. Kraaijveld set his flies selected for wasp-fighting in competition against regular flies for food and found that they fared badly. They grew more slowly than the flies that were still vulnerable to the wasps, they died young more often, and when they grew into adults they were smaller. Evolution doesn’t have an infinite arsenal to offer hosts, and at some point they have to relent, to accept that parasites are a fact of life.

When Darwin set out to write The Origin of Species, figuring out how natural selection works wasn’t his ultimate goal. It was really only a means to an end—to explain the title of his book. After branching and growing for 4 billion years, the tree of life today wears a heavy crown. Scientists have found 1.6 million species, and they may be only a sliver of Earth’s full diversity, which may be many times larger. Darwin wanted to know how that diversity came to be, but he didn’t know enough about biology to find the answer. Now that scientists have a better understanding of heredity and how genes rise and fall over the generations, they’re closing in on how species actually come into being. And they’re finding that the race between hosts and parasites is crucial once again. It may account for much of life’s dense evolutionary canopy.

A new species is born out of isolation. A glacier may cut off a pocket of mice from the rest of their species, and over the course of thousands of years they may develop mutations that make them unlike the rest of the mice and unable to mate with them. A single species of fish may come into a lake and some of its members may start specializing in feeding on the mucky bottom, others in the clear shallows. As they evolve equipment for each kind of life, crossbreeds will turn out badly suited to either one. Natural selection will push them apart, and they will stay more and more with their own until they form separate species.

The life of a parasite encourages new species to form. Parasites can adapt to a single nook in a host—a curl of the intestines, the heart, the brain. A dozen parasites can specialize on the gill of a fish and subdivide it so precisely that there’s no competition between them. Specializing on particular host species makes parasites even more diverse. A coyote will eat just about anything on four legs, and partly as a result, there is only one species of coyote in all of North America. Unlike coyotes and other predators, many parasites are under the Red Queen’s control. A parasite that prefers many different hosts has to try to play the Red Queen game with all of them, like a chess player running frantically between a dozen games he’s playing at once. If another parasite should undergo a mutation that makes it prefer only one host, all of its evolutionary effort will be focused on that host alone. The hosts don’t even have to be an entire species—if just a population of the host is isolated enough, it will pay for the parasite to specialize only on them. With parasites focusing so much on a species or a fraction of a species, they leave room for other parasites to evolve.

As new species are born older ones are going extinct. Species disappear when they are outcompeted, when their numbers shrink down below a critical threshold, or when the world changes too quickly for them to adapt. Lineages of parasites may be able to resist extinction better than those of free-living creatures. While parasites tend to be specialists, they also dabble a little from time to time. Sometimes a new host will turn out to be a good home, and the parasite may found a new species. Tetrabothriid tapeworms are still with us, living in puffins and gray whales, for example, but the pterosaurs and ichthyosaurs in which they lived 70 million years ago are not. The diversity of parasites is like a great lake, with big streams of new species flowing in but only a trickle flowing out into extinction.

Take all these reasons together, and it’s not so surprising that there are so many species of parasites. There are about four thousand species of mammals, and aside from a few rabbits and deer waiting in some obscure forest to be discovered, that number is firm. But there are five thousand species of tapeworms known so far, and new species are discovered every year. There are two hundred thousand species of parasitic wasps. The insects that are parasites of plants number in the hundreds of thousands as well. Add them all up, and the majority of animals are parasitic. Untold thousands of fungi, plants, protozoa, and bacteria also proudly bear the title of parasites.

It’s now becoming clear that parasites may have pushed their hosts to become more diverse as well. Parasites don’t attack an entire species in the same way. The parasites in a particular region can specialize on that population of hosts, adapting to that local set of host genes. The hosts evolve in response—but only the hosts in that region, not the species as a whole. This local struggle has produced some of the fastest cases of evolution ever documented—whether they be yucca moths and the flowers where they lay their eggs, snails and their flukes, or flax and their fungi. And as these populations of hosts fight off their dedicated parasites, they become genetically distinct from the rest of their species.

But this is actually only one way of many that parasites may be able to help turn their hosts into new species. Genetic parasites can speed up the evolution of their hosts, for instance. In order for evolution to take place, genes have to take on new sequences. That can happen with ordinary mutations—the occasional cosmic ray from outer space slamming into DNA or the sloppy crossing of genes as cells divide. But it can happen faster with the help of a genetic parasite. As it hops from chromosome to chromosome within a cell, or as it leaps from species to species, it can wedge itself into the middle of a new gene. This sort of rude arrival usually causes trouble, in the same way throwing a random string of commands into the middle of a computer program does. But every now and then, the disruption turns out to be a good thing, evolutionarily speaking. An interrupted gene may suddenly become able to make a new kind of protein that does a new sort of job. The blind jump of one genetic parasite seems to have made us able to fight parasites more effectively. The genes that make the receptors on T and B cells show signs of having been created out of the blue by genetic parasites.

And once a genetic parasite has established itself in a new host, it can disrupt the unity of the entire species. The typical fate of a genetic parasite is to explode through its host’s genome during the succeeding generations, wedging itself into thousands of sites. As time passes, the hosts that carry it will diverge on their own into separate populations—not distinct species, but groups that tend to breed among themselves. As they do, the genetic parasite continues to hop from place to place in their DNA. Its hopping will be different in each population, and it will make their genes more and more different from one another. Eventually, when a Romeo and Juliet from the two populations meet and try to mate, their distinct collections of genetic parasites may make them incompatible. By making it harder for different populations of their hosts to mix their genes, the genetic parasites encourage them to split into new species.

Another way parasites might be able to create a new species is by mucking up the sex lives of their hosts. A bacterium called Wolbachia lives in 15 percent of all insects on Earth as well as many other invertebrates. It lives within its host’s cells, and the only way it can infect a new host is by colonizing a female’s eggs. When the egg that Wolbachia lives inside becomes fertilized and grows into an adult, it grows up with a case of Wolbachia infection.

There’s a downside to this way of life: if Wolbachia should grow up in a male it faces a dead end, because there are no eggs for it to infect. As a result, Wolbachia has taken control of its hosts’ sex lives. In many of its host species, it tampers with the sperm of infected males so that they can successfully mate only with Wolbachia-carrying females. If one of these infected males should try to mate with a healthy female, all of their offspring will die. Wolbachia uses a different strategy in some species of wasps: normally these insects are born as males and females, which reproduce sexually, but when Wolbachia infects them, the wasps become female-only, able to mother only more females. By turning its hosts all female, the bacteria gives itself that many more hosts.

In both these cases, Wolbachia genetically isolates the infected hosts from the uninfected ones. A newly born host will be the offspring of either Wolbachia-carrying parents or two healthy ones. It won’t be a healthy-unhealthy hybrid. By setting up this reproductive wall, the parasite may be able to set the stage for a new species to form. Wolbachia is only the best-known parasite out of many that tamper with their hosts’ sex lives, so this may turn out to be a common way new species form.

Darwin always had a sharp sense of irony, but this one might have been too much for him to bear. To understand how life changes its form, how evolution is driven forward, and how new species come to be, he could have found inspiration in his dying children. When it comes to the tapestry of life, parasites are a hand at the loom.