Blogs / The Loom

My post on zombie roaches and brain surgeon wasps seems to have hit a nerve. There have been well over 100,000 hits on that post alone, and 175 comments have been posted. I imagine that most people haven’t read through all 175 (many of which have more to do with God than wasps). But I would urge any interested readers to check out
this one from Gal Haspel, who spent seven years in grad school contemplating the sinister glory of Ampulex compressa.

Update 2/15: Gal is now fielding questions in the comment thread, discussing new research on matters such as how the wasp knows where in the brain to put its stinger. Fascinating stuff. Please post any relevant questions for him. Bear in mind, though, that he’s a neuroscientist, not a theologian.

Many thanks, Gal.

I collect tales of parasites the way some people collect Star Trek plates. And having filled an entire book with them, I thought I had pretty much collected the whole set. But until now I had somehow missed the gruesome glory that is a wasp named Ampulex compressa.

As an adult, Ampulex compressa seems like your normal wasp, buzzing about and mating. But things get weird when it’s time for a female to lay an egg. She finds a cockroach to make her egg’s host, and proceeds to deliver two precise stings. The first she delivers to the roach’s mid-section, causing its front legs buckle. The brief paralysis caused by the first sting gives the wasp the luxury of time to deliver a more precise sting to the head.

The wasp slips her stinger through the roach’s exoskeleton and directly into its brain. She apparently use ssensors along the sides of the stinger to guide it through the brain, a bit like a surgeon snaking his way to an appendix with a laparoscope. She continues to probe the roach’s brain until she reaches one particular spot that appears to control the escape reflex. She injects a second venom that influences these neurons in such a way that the escape reflex disappears.

From the outside, the effect is surreal. The wasp does not paralyze the cockroach. In fact, the roach is able to lift up its front legs again and walk. But now it cannot move of its own accord. The wasp takes hold of one of the roach’s antennae and leads it–in the words of Israeli scientists who study Ampulex–like a dog on a leash.

The zombie roach crawls where its master leads, which turns out to be the wasp’s burrow. The roach creeps obediently into the burrow and sits there quietly, while the wasp plugs up the burrow with pebbles. Now the wasp turns to the roach once more and lays an egg on its underside. The roach does not resist. The egg hatches, and the larva chews a hole in the side of the roach. In it goes.

The larva grows inside the roach, devouring the organs of its host, for about eight days. It is then ready to weave itself a cocoon–which it makes within the roach as well. After four more weeks, the wasp grows to an adult. It breaks out of its cocoon, and out of the roach as well. Seeing a full-grown wasp crawl out of a roach suddenly makes those Alien movies look pretty derivative.

I find this wasp fascinating for a lot of reasons. For one thing, it represents an evolutionary transition. Over and over again, free-living organisms have become parasites, adapting to hosts with exquisite precision. If you consider a full-blown parasite, it can be hard to conceive of how it could have evolved from anything else. Ampulex offers some clues, because it exists in between the free-living and parasitic worlds.

Amuplex is not technically a parasite, but something known as an exoparasitoid. In other words, a free-living adult lays an egg outside a host, and then the larva crawls into the host. One could easily imagine the ancestors of Ampulex as wasps that laid their eggs near dead insects–as some species do today. These corpse-feeding ancestors then evolved into wasps that attacked living hosts. Likewise, it’s not hard to envision an Ampulex-like wasp evolving into full-blown parasitoids that inject their eggs directly into their hosts, as many species do today.

And then there’s the sting. Ampulex does not want to kill cockroaches. It doesn’t even want to paralyze them the way spiders and snakes do, since it is too small to drag a big paralyzed roach into its burrow. So instead it just delicately retools the roach’s neural network to take away its motivation. Its venom does more than make roaches zombies. It also alters their metabolism, so that their intake of oxygen drops by a third. The Israeli researchers found that they could also drop oxygen consumption in cockroaches by injecting paralyzing drugs or by removing the neurons that the wasps disable with their sting. But they can manage only a crude imitation; the manipulated cockroaches quickly dehydrated and were dead within six days. The wasp venom somehow puts the roaches into suspended animation while keeping them in good health, even as a wasp larva is devouring it from the inside

Scientists don’t yet understand how Ampulex manages either of these feats. Part of the reason for their ignorance is the fact that scientists have much left to learn about nervous systems and metabolism. But millions of years of natural selection has allowed Ampulex to reverse engineer its host. We would do well to follow its lead, and gain the wisdom of parasites.

Update 2/4/06 4 pm: Greetings to visitors from Slashdot and Boing Boing and other kind linkers. Apologies for the slow load that comes with a surge in traffic. One nice thing about books is that you don’t need a server to turn the pages for you. So if you want more tales of parasitic majesty, check out Parasite Rex.

Update 2/13/06 1 am: Be sure to check out comments from one of the scientists who studies these beasts.

Update 2/15: Gal Haspel is now fielding questions in the comment thread, discussing new research on matters such as how the wasp knows where in the brain to put its stinger. Fascinating stuff. Please post any relevant questions for him. Bear in mind, though, that he’s a neuroscientist, not a theologian.

Many thanks, Gal.

Are brain parasites altering the personalities of three billion people? The question emerged a few years ago, and it shows no signs of going away.

I first encountered this idea while working on my book Parasite Rex. I was investigating the remarkable ability parasites have to manipulate the behavior of their hosts. The lancet fluke Dicrocoelium dendriticum, for example, forces its ant host to clamp itself to the tip of grass blades, where a grazing mammal might eat it. It’s in the fluke’s interest to get eaten, because only by getting into the gut of a sheep or some other grazer can it complete its life cycle. Another fluke, Euhaplorchis californiensis, causes infected fish to shimmy and jump, greatly increasing the chance that wading birds will grab them.

Those parasites were weird enough, but then I got to know Toxoplasma gondii. This single-celled parasite lives in the guts of cats, sheddding eggs that can be picked up by rats and other animals that can just so happen be eaten by cats. Toxoplasma forms cysts throughout its intermediate host’s body, including the brain. And yet a Toxoplasma-ridden rat is perfectly healthy. That makes good sense for the parasite, since a cat would not be particularly interested in eating a dead rat. But scientists at Oxford discovered that the parasite changes the rats in one subtle but vital way.

The scientists studied the rats in a six-foot by six-foot outdoor enclosure. They used bricks to turn it into a maze of paths and cells. In each corner of the enclosure they put a nest box along with a bowl of food and water. On each the nests they added a few drops of a particular odor. On one they added the scent of fresh straw bedding, on another the bedding from a rat’s nests, on another the scent of rabbit urine, on another, the urine of a cat. When they set healthy rats loose in the enclosure, the animals rooted around curiously and investigated the nests. But when they came across the cat odor, they shied away and never returned to that corner. This was no surprise: the odor of a cat triggers a sudden shift in the chemistry of rat brains that brings on intense anxiety. (When researchers test anti-anxiety drugs on rats, they use a whiff of cat urine to make them panic.) The anxiety attack made the healthy rats shy away from the odor and in general makes them leery of investigating new things. Better to lie low and stay alive.

Then the researchers put Toxoplasma-carrying rats in the enclosure. Rats carrying the parasite are for the most part indistinguishable from healthy ones. They can compete for mates just as well and have no trouble feeding themselves. The only difference, the researchers found, is that they are more likely to get themselves killed. The scent of a cat in the enclosure didn’t make them anxious, and they went about their business as if nothing was bothering them. They would explore around the odor at least as often as they did anywhere else in the enclosure. In some cases, they even took a special interest in the spot and came back to it over and over again.

The scientists speculated that Toxoplasma was secreted some substance that was altering the patterns of brain activity in the rats. This manipulation likely evolved through natural selection, since parasites that were more likely to end up in cats would leave more offpsring.

The Oxford scientists knew that humans can be hosts to Toxoplasma, too. People can become infected by its eggs by handling soil or kitty litter. For most people, the infection causes no harm. Only if a person’s immune system is weak does Toxoplasma grow uncontrollably. That’s why pregnant women are advised not to handle kitty litter, and why toxoplasmosis is a serious risk for people with AIDS. Otherwise, the parasite lives quietly in people’s bodies (and brains). It’s estimated that about half of all people on Earth are infected with Toxoplasma.

Given that human and rat brains have a lot of similarities (they share the same basic anatomy and use the same neurotransmitters), a question naturally arose: if Toxoplasma can alter the behavior of a rat, could it alter a human? Obviously, this manipulation would not do the parasite any good as an adaptation, since it’s pretty rare for a human to be devoured by a cat. But it could still have an effect.

Some scientists believe that Toxoplasma changes the personality of its human hosts, bringing different shifts to men and women. Parasitologist Jaroslav Flegr of Charles University in Prague administered psychological questionnaires to people infected with Toxoplasma and controls. Those infected, he found, show a small, but statistically significant, tendency to be more self-reproaching and insecure. Paradoxically, infected women, on average, tend to be more outgoing and warmhearted than controls, while infected men tend to be more jealous and suspicious.

It’s controversial work, disputed by many. But it attracted the attention of E. Fuller Torrey of the Stanley Medical Research Institute in Bethesda, Maryland. Torrey and his colleagues had noticed some intriguing links between Toxoplasma and schizophrenia. Infection with the parasite has been associated with damage to a certain class of neurons (astrocytes). So has schizophrenia. Pregnant women with high levels of Toxoplasma antibodies in their blood were more likely to give birth to children who would later develop schizophrenia. Torrey lays out more links in this 2003 paper. While none is a smoking gun, they are certainly food for thought. It’s conceivable that exposure to Toxoplasma causes subtle changes in most people’s personality, but in a small minority, it has more devastating effects.

A year later, Torrey and his colleagues discovered one more fascinating link. They raised human cells in Petri dishes and infected them with Toxoplasma. Then they dosed the cells with a variety of drugs used to treat schizophrenia. Several of the drugs–most notably haloperidol–blocked the growth of the parasite.

So Fuller and the Oxford scientists joined forces to find an answer to the next logical question: can drugs used to treat schizophrenia help a parasite-crazed rat? They now report their results in the Proceedings of the Royal Society of London (press release). They ran the original tests on 49 more rats. Once again, parasitized rats lost their healthy fear of cats. Then the researchers treated the rats with haloperidol and several other anti-psychotic drugs. They found that the drugs made the rats more scared. They also found that the antipsychotics were as effective as pyrimethamine, a drug that is specifically used to eliminate Toxoplasma.

There’s plenty left to do to turn these results into a full-blown explanation of parasites and personalities. For example, what is Toxoplasma releasing into brains to manipulate its hosts? And how does that substance give rise to schizophrenia in some humans? And even if the hypothesis does hold up, it would only account for some cases of schizophrenia, while the cause of others would remain undiscovered. But still…the idea that parasites are tinkering with humanity’s personality–perhaps even giving rise to cultural diversity–is taking over my head like a bad case of Toxoplasma.

Update 2/9: link to new PRSL paper fixed.

One of the most exciting lines of research in evolution today is how parasites have become so good at making us sick. A case in point appears in the latest issue of Genome Biology (full text of paper here). It appears that parasites have stolen one of our best lines of defense and now use it against us.

When bacteria or other pathogens try to invade our bodies, we marshall an awesome system of biochemistry to ward them off. Recently, a group of French and German molecular biologists took a look at a key piece of that system, a molecule studding the surface of our cells called alpha-2-macroglobulin. Parasites penetrate a host cell by releasing enzymes that can punch a hole through the cell wall. But alpha-2-macroglobulin can snag these enzymes before they do damage, tucking them away in a cage where they can be destroyed.

You can find the gene for alpha-2-macroglobulin not only in humans but in other animals. The French and German researchers have identified a number of other versions of the gene in invertebrates by trawling through genome databases, looking for sequences that are similar to the alpha-2-macroglobulin gene. In some cases, other animals have evolved much more sophisticated variations on this particular defense than we have. Mosquitoes, for example, use 15 different versions of the gene. When you suck blood for a living, there’s a high premium on eradicating the parasites you slurp up as well.

It is now clear that the common ancestor of all animals on Earth evolved an ancestral version of alpha-2-macroglobulin, which was then passed down and gradually altered over a billion years of animal evolution. But the European researchers found some surprises as they hauled up their genomic nets. They found many versions of the alpha-2-macroglobulin gene in bacteria as well. Not in all bacteria, mind you, but in a wide range of species, most of which live inside animals. When the researchers looked at a family tree of bacteria, the ones carrying versions of alpha-2-macroglobulin were scattered across its branches. In many cases, their closest relatives lacked the gene.

Here’s the hypothesis that the researchers came up with to explain this weird pattern. An early animal equipped with alpha-2-macroglobulin was infected with a bacterium. The microbe accidentally acquired the animal gene and wove it into its own genome. (This has been documented happening many times among bacteria. They can scoop up genes from dead microbes, and viruses hopping between bacteria can deliver genes as well. But the exchange from animals to microbes hasn’t been studied very well till now.)

The stolen alpha-2-macroglobulin gene turned out to give the pathogen an advantage over others that lacked the gene. Specifically, it was able to use this host-defense molecule to defend itself from the host. It just so happens that animals also use enzymes to punch holes in the cell walls of their enemies. But while bacteria punch holes to invade a cell, animals do so in order to rip open pathogens and kill them. After one species of bacteria stole the alpha-2-macroglobulin gene from animals, it began to use the gene to trap their host’s hole-punchers. Later, it handed off the gene to other species of bacteria also living in animal cells. They also used it to defend themselves against their hosts.

The scientists point out that they still have to rule out the possibility (unlikely as they consider it) that the transfer went the other way: that animals acquired their alpha-2-macroglobulin defense from bacteria. But there’s a straightforward way to do that. They need to make a large-scale comparison of the version of the gene in bacteria, as well as in animals. If they’re right, then the tree will show that all of the bacterial versions descend from animal versions of the gene. If they’re wrong, the opposite pattern will emerge.

Either result would, however, point to one important conclusion: gene-swapping has been a big deal in the history of life. Scientists have known for a long time that it’s important for the rise of antibiotic resistance in bacteria. They’ve also known that the energy-generating mitochondria of our cells are actually captured degenerate bacteria. But it was hard to know how important gene-swapping was beyond these examples until entire genomes became available for study. When scientists first began to analyze genomes for evidence of gene-swapping, they sometimes claimed evidence for it that disappeared when more data came in. The most glaring example came in 2001, with the publication of the rough draft of the human genome. The authors of the draft claimed that a few percent of the human genome consisted of genes imported from bacteria. A comparison with more genomes later showed that this was not true.

The Genome Biology paper is an example of today’s more thorough tests for gene-swapping. (In this case, they studied 32 species of bacteria, not to mention a wide range of animals.) It’s also an example of why this sort of research matters. Bacterial versions of alpha-2-macroglobulin could become excellent targets for drugs that would prevent the microbes from defending themselves against our hole-punching.

Few humans have been as successful in Hollywood as parasitoids. Parasitoids are a particularly gruesome kind of parasite that invariably kills its host by the time it becomes an adult and is ready to leave the host’s body. A parasitoid female wasp, to give one example, will fly along until it finds a caterpillar of some particular species. It lands on top of the caterpillar, jabs an egg-laying stinger into the caterpillar’s body, and injects some eggs. The eggs hatch, the wasp larvae feed on the living caterpillar from within, and then, when they’re ready to metamorphose into adults, they crawl out of their hapless host, leaving it to die.

The screenwriter Dan O’Bannon reportedly had nightmares about parasitoids, and out of those dreams emerged a script about an alien that laid its eggs inside human hosts, which then burst out of their hosts’ chests. In 1979 that script became the movie Alien. Fifteen years later, with three sequels out and Alien 5 reportedly in the works, this oversized parasitoid is a genuine star. If Mary Kate and Ashley Olson have their own star on the Hollywood Walk of Fame, then surely there is room for the imprints of this creature’s claws.

Alien 5 is rumored to be about the arrival of parasitoid aliens on Earth. Actually, they’re already here, and they’ve won the battle. There are at least 200,000 species of parasitoid wasps alone, along with many more species of flies and other insects. They’re not limited to some island off of Madagascar–they’re found around the world, in deserts, jungles, and the tomato plants in your garden. They consume the minds of a large army of entomologists, who document their awesome, chilling success. I had a great time writing about parasitoids as part of my 2000 book Parasite Rex, but the science of parasitoids has continued to march forward. The 2004 issue of Annual Reviews of Entomology has just come out, and it has three reviews that sum up what scientists know about them so far.

Hundreds of different insect lineages have evolved into parasitoids, and so they’ve acquired a head-spinning diversity of ways of taking advantage of their hosts. Some parasitoids lay their eggs in the neighborhood of their particular host, and when the egg hatches, the larva may crawl, skitter, or squirm around for weeks until it finds one. Parasitoids can be very picky in the hosts they choose. They can measure how big a potential host is, and will reject ones that are too small. They can also tell if there are already parasitoids living inside. (Remember that alien in Alien Resurrection sniffing Sigourney Weaver and then sparing her?) If parasitoids determine they’ll have good odds looking for a fresh host, they’ll skip a parasitized host, but if options are few, they’ll move in as well. In one wasp species, the larvae will normally drill their way into a caterpillar’s back. If they sense that there’s another wasp inside, they’ll drill into its underside so as to delay a confrontation. And these confrontations do get ugly. Some species even produce special castes of killers that prowl the interior of a host, destroying any parasitoids that are not their own siblings. And once the invaders are gone, the killers go after their brothers since only a few males can keep their lineage alive.

Meanwhile, the parasitoids begin to manipulate their hosts. They need to fend off the immune system or die; in many cases, the host undergoes a kind of insect AIDS in which they can no longer fight against parasites. In other cases, the parasitoid manages to camouflage itself from attack. Some parasitoids immediately paralyze a caterpillar, chew up its insides quickly, and crawl out of the cadaver. Others play it slow. They develop over weeks, and allow their host to go on munching on leaves. As those leaves get turned into fluids, the parasitoids slurp them up. They hijack their host’s physiology, preventing them from storing up energy as fat. In order to hold onto to this sweet living arrangement as long as possible, they have to stop their host from building a cocoon and turning into a moth or some other adult form. They do so by adjusting the flux of hormones in the host’s body, so that it just keeps growing into an oversized infant.

Perhaps you remember John Hurt in the original Alien. An alien jumped on his face (see the picture above) and then, unbeknownst to the crew, it inserted itself into his body. The only clue that something was amiss was that Hurt was voracious. It makes sense for the alien to get Hurt to bring it some food. It makes sense for real parasitoids, too. Parasitoids do more than make their hosts hungry. Spiders will weave webs before they die that are especially suited for supporting a parasitoid wasp’s cocoon. Some caterpillars will crawl to the ground and burrow into a hole, giving the parasitoids a safe refuge for the winter. When aphids are hosts to parasitoid wasps, they will crawl to the tops of plants, away from the other aphids and the predators that feed on them. There, the wasp kills the aphid, which becomes nothing but a hollow mummy inside which the wasp makes its cocoon. If a parasitoid is born late in the year and will have to hibernate through the coming winter, the aphid will find a well-protected spot instead.

Parasitoids achieve all this with cocktail of hormones, proteins, and genes that take over the workings of their host’s body. Some of these compounds are made by the parasitoid larva itself. In the case of many parasitoid wasps, other compounds come from the venom the mother injects with her eggs. Others come from some extraordinary viruses that the mothers also inject. These viruses aren’t really viruses in the conventional sense. Their genetic code is part of the parasitoid genome, existing in every cell of every wasp. When females prepare to lay eggs, these DNA sequences splice themselves out of the genome and get packaged in protein shells. And when they enter the host, they invade the host’s cells. In some cases, they act like HIV, disabling the immune system. In other cases, they help stop the host from entering metamorphosis. In the process, they are committing a sort of viral suicide, because they will die with their host. But on balance, there’s an advantage to the genes, because they promote the spread of more viruses by helping the wasps.

There are lots of very practical reasons to study parasitoids. They are far more sophisticated at altering the biochemistry of pests than we are, and they’re now a mainstay in biological control. It might even be possible to use the genes of their viruses to create hybrid viruses that can be sprayed onto crops, or perhaps even past the genes into the genomes of the plants themselves. But there are more profound reasons to contemplate parasitoids as well. Parasitoids have had a special place in our imagination long before O’Bannon’s bad dreams. In a letter, Charles Darwin wrote “I cannot persuade myself that a beneficent and omnipotent God would have designedly created the Ichneumonidae [a group of parasitoid wasps] with the express intention of their feeding within the living bodies of Caterpillars.” The same holds true today. I have yet to hear from the Intelligent Design camp what the exquisitely complex cruelty of parasitoids tells us about the Designer who tailor-made them.

But it’s the parasitoid viruses that trigger the most musings. What are they? What name can do them justice? Some biologists have proposed that they descend from ordinary viruses that got accidentally pasted into parasitoid genomes, and then began to serve their host. If that’s true, how is it that the viruses contain genes that are common to many insects, producing proteins that help carry information from the surface of a cell to the DNA and back again? Others have suggested that these viruses are actually pieces of so-called “jumping DNA”–native genetic sequences with a knack for inserting copies of themselves around the parasitoid genome. Add a couple genes for making a protein shell, and they’re ready for service. Are they Richard Dawkins’s extended phenotype? Is it the wasp that is infecting its host’s cells? Can an animal make itself into a viral disease? If not, just where does the parasitoid stop and its virus begin? It would be nice if Alien 5 could ponder mysteries like these, but somehow I doubt it will.

(Update 1/8/03 Thanks to Jeff Boettner at UMass for correcting my definition of parasitoids.)

Biologists these days can paint many different portraits of the same organism. They can follow the tried and true style of Aristotle and paint with a broad brush, describing what they can see with the naked eye–number of legs, color of hair, live young or eggs. Or they can paint a creature at the cellular level–the twist and turns of collagen fibers in a horse hoof or the poison-producing organelles of a rattlesnake. In the past few years a new kind of portrait has been hung in the biological museum: a portrait of the genome. In the thousands or millions of DNA base pairs, genomes can reveal secrets not only about an organism’s natural history, but its ancient history as well.

Some genomes are big (ours is over 3 billion base pairs). Others are small. Today saw the unveiling of the portrait of the smallest genome of a cellular organism ever sequenced. At only 490,000 base pairs, the genome of the microbe Nanoarchaeum equitans is less than a thousandth the size of the human genome. It’s a portrait in miniature, but like all great miniatures, it is packed with exquisite details.

N. equitans is new to science. In 2002, explorers searching the hydrothermal vents off the coast of Iceland discovered microbes covered by tiny balls. On closer inspection, the balls turned out to be microbes themselves measuring just 400 nanometers across. At first glance, it looked as if N. equitans was a parasite on the bigger microbe.

Parasites are nothing unusual, but when scientists studied how it fit into the tree of life, it became clear that N. equitans was certainly unusual. All living things belong to one of three great domains. We humans (along with plants, mushrooms, and amboebas) are eukaryotes. Most of the microbes we’re familiar with (particularly by making us sick) are bacteria. But there’s a third domain scientists have only recognized in recent years, called Archaea. Archaea can thrive in oxygen-starved swamps, salt flats, and other harsh environments. The deepest-branching lineages of the Archaea are generally found around hydrothermal vents. This may be because life got its start in the scorching waters at the seams of the Earth.

N. equitans, it turns out, is an Archaea–the first Archaean parasite ever found. But even more astonishingly, it sits on a branch that reaches down to the very base of the Archaea. It’s a relict of the earliest chapters of life, over three billion years ago.

It’s easy to prejudge the signficance of N. equitans. Its tiny genome might suggest that it is a degenerate that has lost most of its genes as it has enjoyed the decadence of the parasite’s life. On the other hand, its ancient heritage might suggest that its genome shows us what life was like in its earliest stages, before it had become very complex. If you chose either of these possibilities, you’d be wrong.

In a paper appearing this week in the online edition of the Proceedings of the National Academy of Sciences, a team of researchers show that N. equitans turns out to be something else altogether. Its genome is tight, efficient, and surprisingly complex. Our genomes may be big, but it’s full of junk. Only about 2% of it is actual genes; much of the rest of it is composed of defunct genes and virus-like sequences of DNA. N. equitans, on the other hand, has hardly any junk DNA at all. Almost its entire genome is made up by its 552 genes.

It’s also true that the genome of N. equitans lacks genes for basic jobs like synthesizing amino acids and lipids–stuff that it can steal from its host. But on the other hand, the microbe makes lots of enzymes involved in processing the information in its genome. It can even read out two parts of a gene located on different chromosomes and stitch the result together into a single protein.

It will take a lot of research figure out the full significance of this new portrait, but I think it already shows something very important about biology–something I stressed in my book Parasite Rex: the genomes of parasites are not the dustbins of history but the jewels of evolution.

As someone who writes a lot about evolutionary biology, I’ve often had people say to me, “I just can’t believe that evolved.” Originally, that referred to the lovely side of nature–the beauty of flowers, for example, or the grace of birds in flight. The implication was that these things were so beautiful and intricate that they had to be created for a purpose–a beautiful purpose, obviously.

But after I started writing about parasites, that underwent a fascinating change. Parasites may be deadly and gross, but they also have some mind-boggling adaptations. Most mind-boggling of all is the way many species travel through two or more hosts during their life cycle. Some flukes live first in snails, which cough them up in slime balls, then in the ants that eat the slime balls. Then the flukes drive the ants up a blade of grass, so that they can be eaten by sheep and cows, their final host. There they mate and lay eggs, which then get passed out with the host’s dung. Tapeworms live in cows and pigs, and then in humans.

When people find out about these creepy life-cycles, they emphatically say, “I just can’t believe that evolved.”

That that fascinates me. It reminds me of the way tapeworms were used to prove God’s wisdom in the 1800s. At the time people didn’t realize that tapeworms lived first in cows and pigs, and then in humans. They had some similarities in both hosts, but in us, they’re long and skinny, while in cows and pigs they look like little buttons with fringes of hooks. So some scientists claimed that the tapeworms in cows and pigs were deformed dead-enders in the wrong host. This outraged a devout German doctor named Friedrich Kuchenmeister (a name that invites repeated utterances, I can tell you). Kuchenmeister declared that dead-end tapeworms would be “contrary to the wise arrangement of Nature.” He had the brilliant idea that tapeworms went through two hosts. To prove his case, he plucked the button-shaped tapeworms out of a roast pork and fed them in a soup to a criminal about to be executed. After the man was hanged, Kuchenmeister slit open his intestines and discovered the tapeworms maturing into their long, skinny form. Kuchenmeister found a gruesome vindication of his faith (and made a major biological discovery).

It is certainly hard–at first–to imagine how a parasite could evolve from a single host to two or more–including ones as different as snails, ants, and sheep. After all, parasites are exquisitely adapted to their hosts, able to hijack their metabolism, evade their immune system, and sometimes manipulate their brains. So how could a parasite so well adapted to one host evolve to live inside a completely different one. It seems too complex a pattern. It invites the idea that it must have been designed. But what does this mean about the designer of these parasites? That it/he/she gets personally involved in making parasites into exquisitely sophisticated killers, that it/he/she revels in the baroque sadism of these creatures?

Fortunately, the evolution of parasite life cycle is not incomprehensible. This week biologists from the University of Liverpool mapped out some interesting new ideas about how parasites find new hosts. There’s a lot of mathematical modeling and parasitological minutae in the paper, but the key is that in most cases, multiple hosts are linked together in food webs. In other words, one eats the other.

Here’s a simplified scenario that gives you the gist of their argument. Imagine millions of years ago there’s a species of tapeworm that lives only in wildebeest. Fairly often, its hosts get killed by lions. The tapeworms that die with their wildebeest host can no longer reproduce. So now there’s an automatic edge for any parasite that can manage to survive a lion attack. Perhaps the first mutations allowed a tiny fraction of the tapeworms eaten by lions to escape with the lion’s droppings. Over time, these mutations would become more common because they boosted the tapeworm’s chances of reproducing.

As the tapeworms evolved better strategies for surviving in the lions, evolution would begin to favor the ones that could feed on the lion as well as the wildebeest. After all, here’s a big, long-lived host who can provide a massive food supply to any parasite that can survive in its gut. So the tapeworms start adapting to the lions as well. After a while, the tapeworms hold off on developing into their adult form until they get into the lion, so that they can take full advantage of their new host. Over time, the wildebeest stage of the parasite comes to look almost completely different from the adult.

Not all parasites can jump into new hosts this way. They have to be able to navigate that intermediate stage, when they can complete their lifecycle in either wildebeest and lions, for example. But as the Liverpool team points out, there are plenty of examples of parasites today that can switch-hit this way.

Ultimately, this research is important not for debates about the wisdom vs the sadism of God’s creation, but as medicine. We humans, are the final host not only for tapeworms, but for lots of other parasites, including blood flukes (also carried by snails) and Plasmodium, the mosquito-borne source of malaria. These diseases each have histories of their own, as parasites built up their life cycles and then modified them by switching from one host to another. And new ones will keep coming into existence, so we have to be prepared. You can believe that that didn’t evolve, but do so at your peril.