Parasite Rex: Inside the Bizarre World of Nature's Most Dangerous Creatures

2 Terra Incognita

Raquel Welch would have fared pretty poorly without her submarine. Suppose she had been shrunk down to the size of a pinhead and then had to get into the bloodstream of the dying diplomat on her own. Even if she could have clawed her way through the tough layers of skin and wiggled into a blood vessel, she would then have been sent flailing through his circulatory system by the pulsing push of his heart. Let’s say, for the sake of argument, that she could wear a scuba-like mask that could pull the oxygen out of the blood so she could breathe. She’d still suffocate if she ended up in some part of the body where there’s hardly any oxygen at all, like the liver. And as she tumbled through the darkness she’d be utterly lost, with no idea whether she was in the vena cava or the carotid artery.

The inside of a body is a tough place to survive. With our air-breathing lungs, our ears finely tuned to the vibrations of the air, we are adapted to life on land. A shark is made for the sea, ramming water through its gills and smelling for prey miles away. Parasites live in a different habitat altogether, one for which they are precisely adapted in ways that scientists only barely understand. Parasites can navigate through their murky labyrinth; they can glide through skin and gristle; they can pass unscathed through the cauldron of the stomach. They can turn just about every organ in the body—the eustachian tube, the gill, the brain, the bladder, the Achilles tendon—into their home. They can rebuild parts of the host’s body to suit their own comfort. They can feed on almost anything: blood, gut lining, liver, snot. They can make their host’s body bring them food.

Parasitologists need years, sometimes decades, to decipher these adaptations. They can’t spend a summer following a troop of monkeys or put radio collars on a pack of wolves. Parasites live invisibly, and parasitologists usually can see what they’re doing only by killing their hosts and dissecting them. These grisly snapshots slowly add up to a natural history.

Steenstrup knew that flukes were extraordinary animals, but little more than that. After one hundred fifty years of experiments, parasitologists can show just how extraordinary they are. Consider the blood fluke Schistosoma mansoni, a tiny missile just emerged from its snail and swimming through a pond in search of a human ankle. If it feels the ultraviolet rays of the sun, it stops swimming and sinks back down into the darkness to hide from the damaging radiation. But if it senses molecules from human skin, it begins to swim madly, jerking around in different directions. When it reaches the skin, it drills its way in. Human skin is far tougher than the soft flesh of a snail, so the fluke lets its long tail snap off, the wound quickly healing as it burrows in. Special chemicals it releases from its coat soften up the skin, letting it plunge into its host like a worm in mud.

After a few hours it has reached a capillary. It has traded the streams of the outside world for the internal ones. These capillaries are barely wider than the fluke itself, so the fluke needs to use a pair of suckers to inch forward. It makes its way to a larger vein, and a larger one still, finally making its way into a torrent of blood so powerful it carries the fluke away. The parasite rides the surge until it finally reaches the lungs. It moves from the veins to the arteries like a snake in a forest canopy. Finding its way back into a lung capillary, and then to a major artery, it is swept through the body once again. It may tour its host’s entire body three times until it finally comes to rest in the liver.

Here the fluke lodges itself in a vessel and finally has its first meal since leaving the snail: a drop of blood. It now begins to mature. If it’s a female, a uterus starts to take shape. If it’s a male, eight testes form like a bunch of grapes. In either case, the fluke grows dozens of times bigger in a few weeks. Now it is time for the parasite to search for a partner for life. If it is lucky, other flukes sniffed out this human host and are lodged in the liver as well. The females are delicate and slender; the males are shaped something like a canoe. They begin to make blood-borne odors that lure members of the opposite sex, and once a female encounters a male, she slips into his spiny trough. There she locks in, and the male carries her out of the liver. Over the course of a couple of weeks, the pair make the long journey from the liver to the veins that fan out across the gut. As they travel the male passes molecules into the female’s body that tell her genes to make her sexually mature. They keep traveling until they reach a resting place unique to their own species. Schistosoma mansoni stops near the large intestine. If we were following Schistosoma haemotobium, it would take another route to the bladder. If we were following Schistosoma nasale, a blood fluke of cows, it would take yet another route to the nose.

Once they find their destined place, the fluke couple stay there for the rest of their lives. The male drinks blood with his powerful throat and massages the female to help thousands of blood cells flow into her mouth and through her gut; he consumes his own weight in glucose every five hours and passes on most of it to her. They may be the most monogamous couples in the animal kingdom—a male will clasp onto its female even after she has died. (A few homosexual flukes will also get together. While their fit isn’t as tight, they will keep reuniting if a disapproving scientist should separate them.)

Heterosexual flukes mate every day of their long lives, and whenever the female is ready to lay her eggs, the male makes his way along the wall of the bowels until he finds a good spot. The female slides partially out of the trough, far enough to lay her eggs in the smallest capillaries. Some of the eggs are carried away by the bloodstream and end up back in the liver, that meaty filter, where they lodge and inflame the tissue, causing much of the agony of schistosomiasis. But the rest of the eggs work their way into the intestines and escape their host, ready to slice open their shells and find a new snail.

Each piece of the parasite puzzle costs years of research. The question of how parasites navigate has taken up just about the entire career of one scientist, Michael Sukhdeo. Sukhdeo teaches these days at Rutgers University in New Jersey. New Jersey may be a long way from Tambura, but he has no shortage of parasites to study in horses, cows, and sheep. I paid a visit to Sukhdeo at his office. He is a stocky man with a sly goatee. A bike hangs from his office wall, fish swim in a tank by his desk, and classic rock comes out of his radio. Sukhdeo, like a lot of parasitologists I’ve met, can slide into gruesome conversation without any warning. I suppose when you spend your days studying creatures that chew up the lining of livers and intestines, there’s no sense in dancing around the uglier basics of life. He started to talk about how grotesque it is when people get elephantiasis, which was common in British Guyana, where he spent much of his childhood. “Everywhere you walked you saw people with huge bulges in their crotch and big swollen elephantine feet,” he said.

Sukhdeo then told me how he himself became infected when he was eleven. He developed a swelling, and his parents took him to a clinic. “When you’re testing for elephantiasis, the microfilaria come out into the bloodstream only at dusk. Nobody knows where they go. So at night we had to go to this clinic to get our blood checked. And there was a girl there, about my age; she was eleven, and she had only one breast. That’s a place where the worms live. She was a beautiful girl; I was in love. We both got checked at the same time. It was twelve Guyanese dollars—six American dollars—for treatment. They couldn’t afford it for their daughter. We offered to pay for them, but they were very proud and wouldn’t even take a loan. And so that girl remained infective—over six American dollars.”

Sukhdeo went to McGill University in Montreal, and there he discovered that while parasites might be grotesque, they were also the most interesting creatures he had ever encountered. “I took a course in human parasitology, and—pow—it was disgusting and really exciting. I had gone through four years of university and nothing had turned me on in just that way. They were just so weird, and there was so little known about them.”

He decided to go on studying parasites in graduate school, and there he realized that people had very little idea of how parasites behaved as actual, living organisms. Many parasitologists have resigned themselves to studying them on an abstract plane—cataloging new species according to their suckers and spines, for example, without ever knowing what those suckers and spines are for.

For his master’s degree, Sukhdeo chose Trichinella spiralis. This tiny nematode comes our way inside the muscle of undercooked pork, where it lives in cysts formed from individual muscle cells. When a person eats the meat, the parasite breaks out of its cyst and makes its way into the intestines, threading itself through the cells of the lining. There it mates and produces a new generation of Trichinella, which leave the intestines and travel through the bloodstream until they lodge in the person’s muscle and form cysts of their own. Humans are only accidental hosts for Trichinella; they are unable to carry the parasite on to the next stage of its life cycle. Pigs are a much more profitable host; a dead pig may be scavenged by a rat, which then dies and is scavenged by another rat, which may be eaten by a pig. Pigs can pass Trichinella to each other by being fed infected meat or by chewing their tails off. In the wild, predatory mammals and scavengers keep the cycle spinning along—ranging from polar bears and walrus in the Arctic to hyenas and lions in Africa.

The parasites traveling each of these cycles had been designated as individual species, but no one actually knew whether they weren’t actually a single species scattered among different regions and hosts. Sukhdeo got hold of Trichinella from Russia, from Canada, and from Africa, as he was told, and he ground up each sample and infected mice with them. He extracted the antibodies that the mice’s immune systems produced against the ground-up parasites and compared them to judge how similar they were to one another.

Eventually he stopped to wonder why he was doing what he was doing. His experiments were based on the assumption that individuals of a species look similar to one another. This is usually a pretty reliable assumption, but biologists have recognized that it’s not always the case. Poodles and Dobermans belong to the same species, for instance. On the other hand, two beetles that look practically identical may belong to separate species. Rather than focus on appearances, biologists these days define a species as a group of organisms that breed together and don’t breed with other groups. It’s out of that isolation that evolution then makes a species distinct from others.

Sukhdeo decided that the best way to study the species of his parasites was to work out their sex life. He dissected Trichinella cysts out of muscle and teased out the worms, only 250 microns long. He’d check their sex and then get the parasite into a syringe, which he’d inject into the stomach of a mouse. Then he’d go back to his cysts and find a parasite of the opposite sex, and then inject it into the mouse’s stomach as well. A month later he’d look at the mouse’s muscle to see whether they had mated and produced young.

Sukhdeo concluded that the African form was probably a subspecies and not a separate species of its own. But the experiment actually raised a much deeper, much more interesting question. How did the parasites find each other?

Apply the Fantastic Voyage method: It would be as if you were thrown down into a dark cavernous tunnel twelve miles long, lined on all sides with slippery, tightly packed, man-sized mushrooms. If you were set down randomly in there and moved around randomly, there’d be no hope of finding someone else in such a place. And yet, Trichinella—without a map or even much of a brain—always did.

Sukhdeo wanted to know how they did it, but his adviser told him not to try. “‘You can’t find out how these animals go wherever they go because for a hundred years parasitologists have been trying to find out the answer and they haven’t been able to. Better people than you have tried.’”

Sukhdeo ignored the advice and set out to find the secret to parasite navigation. Unfortunately, he set out in the wrong direction. He assumed that like animals on the outside, parasites must follow a gradient. A shark smells the blood of a wounded seal from miles away and heads for it, thanks not only to its sharp nose but to the simple law of how blood spreads in water. The farther away the blood travels from the seal, the thinner it gets. If a shark keeps heading along a rising gradient, it will automatically reach the source. As soon as it veers away in the wrong direction, the blood trails off, and it can right itself. Gradients work in the air just as well as in the water. They help lead bees to flowers and hyenas to carcasses. Tracking gradients works so well at sea and on land that it only made sense that parasites must use them as well. Parasitologists searched for the scent of a gallbladder, the whiff of an eye. They didn’t find any.

For years, Sukhdeo tried to find the secret for himself. He built chambers out of Plexiglas in which he could put a parasite, and then he’d add different chemicals to see if it would swim toward it. At first he kept his entire lab heated to body temperature. Then he invented a system of tubes to circulate warm water around his artificial gut. “I would try to sample everything they encountered in the host. First I tried salivary secretions, and then I would move down the gut.” Nothing he did made sense. He couldn’t get the parasites to swim toward or away from any substance he put in the chamber.

They did react sometimes, but in a way that made no sense at all. “Whenever these little parasites encountered bile they started moving like crazy,” Sukhdeo said. “That wasn’t what I wanted—I wanted something that attracted them. Initially they would move back and forth fifty times a minute, and if you put bile in, there was an instantaneous change and they started moving sinusoidally.”

Sukhdeo kept looking for the key to parasite navigation after he moved to the University of Toronto. As he searched he drifted into an academic limbo. At Toronto he met his wife, Suzanne, who was also getting her Ph.D. in parasitology with the director of his lab. When the director developed Alzheimer’s disease, Sukhdeo took over the lab and became Suzanne’s dissertation advisor. If he had wanted to have a real career in parasitology, he should have been looking for jobs elsewhere, but instead he lingered in Toronto, applying for more money each year to carry on his experiments. For six years he floated in this dead-end existence, but he found that it gave him the freedom to search for answers that other scientists thought were unreachable. “I had nothing to lose,” Sukhdeo says. “I could do anything I wanted, and I had no future.”

He decided to extend his research to other species, such as the liver fluke, Fasciola hepatica. A relative of the blood fluke, it has a similar life cycle. It lives inside cows and other grazing mammals, and its eggs pass out of its host’s body with feces. It hatches from its egg and swims in search of a snail, where a couple of generations grow up. Cercariae emerge from the snail and swim away from the snail until they hit any object—usually a rock or a plant—and build themselves a tough transparent cyst. When another grazing mammal eats them, their acid-proof shell carries them safely through the stomach and into the intestines. Once in the intestines, they break loose and burrow out into the abdominal cavity and then head for the liver. There they grow into adults—leaf-shaped inch-long animals that can cram into a liver by the hundreds and live for eleven years. Liver flukes can sometimes get into humans, but the real danger they pose is to livestock. In tropical countries, between 30 and 90 percent of cattle carry them, and they cause $2 billion in damage every year. Yet, despite the massive harm they cause and despite decades of research, scientists had no idea how they managed to find the liver.

Sukhdeo built himself new chambers out of brass and aluminum and put liver flukes into them. He spent three years trying out different compounds given off by the liver—chemicals that might lure the flukes to their final home. Out of sheer exasperation, he tracked down a prominent liver physiologist to see if there was some attractant he had overlooked.

“He thought about it for a long time and said, ‘You know, son, around the liver there is a capsule; it’s called Glisson’s capsule?’”

“‘I said, ‘Yes.’

“He said, ‘Well, that’s the end of my universe.’”

Sukhdeo found that while he couldn’t get liver flukes to swim upstream to any particular cue, certain chemicals like bile made them react violently. He had seen the same strange reaction in Trichinella when he exposed it to the chemical pepsin. And then, as he was chewing over his data he realized that he had been looking at the problem from the wrong angle all along. He had been looking at the fluke or worm as a free-living creature, not as a parasite. A body is not a peaceful ocean. It’s a sealed space in which fluids churn and slosh. A scent released from one organ can’t spread smoothly and tranquilly through other organs. An airborne odor spreads out evenly, essentially to infinity, but a chemical marker inside a body must come up against any of a number of barriers, bouncing back and saturating the territory, destroying any clues it might have offered.

Sukhdeo explained his realization to me in his office, waving his arms at the wall. “For a gradient to form, you need an open-ended system, and you can’t have turbulence. If I put a piece of toast here, you would smell it and know where it is. If I closed the room, quickly it would saturate. Because it’s in a closed sysem, you can’t have a gradient. If you put guts in this room, they would do the same thing.”

The world of a parasite isn’t like our own—it has its own constraints and opportunities. Because of the strange conditions found inside a body, Sukhdeo wondered whether parasites might be able to navigate not with gradients but by simply reacting to a few different sorts of stimuli. Konrad Lorenz had shown that free-living animals in the outside world rely on reflexive behaviors when they find themselves in predictable situations. If you’re a goose and one of your eggs starts to roll out of your nest, you can perform a set of automatic actions to get it back: stick out neck, pull back neck, bend head down. That should get the egg under your beak and back into the nest without requiring you to pay much attention to the egg itself. If a biologist should sneak a goose’s egg out from under its beak in the middle of this sequence, the goose will keep pulling its neck back anyway.

Sukhdeo wondered whether parasites relied on these kinds of programmed behavior more than free-living creatures. A body is in some ways more predictable than the outside world. A mountain lion born in the Rockies has to learn the shape of its territory and relearn it whenever a fire or a landslide or a parking lot suddenly changes the topography. A parasite can travel through a rat, safe in the knowledge that it crawls through a little biosphere that’s almost identical with any other rat interior. The heart is always between the lungs, the eyes in front of the brain. By reacting in a certain way to certain landmarks on their journey, parasites can be transported where they need to go. “Everything else is irrelevant,” says Sukhdeo. “They don’t have to waste time generating neurons to recognize everything else that’s going on.”

Now all the weird behavior of Trichinella and liver flukes settled down into straightforward recipes for success. Trichinella sits tight in its muscle capsule as it falls into the stomach. There it picks up one of the chemicals, known as pepsin, that breaks food down in the stomach; in response, Trichinella starts to flail. “The first movement causes them to break out of that cyst. You can see them whipping until the tail lashes out and they’re out in the stomach.” The piece of meat they’re lodged inside passes out of the stomach and into the intestines, where there’s a duct from the liver down which bile flows to help with digestion. And bile is the second trigger, making them change from their whipping movement to a snakelike slither. That lets them move out of the food and into the intestines.

Sukhdeo figured out a way to test this idea. “What if I changed where the bile came in?” he said. “I had learned a lot about surgery, and I could stick a cannula with bile anywhere I wanted.” Wherever along the intestines he moved the source of the bile was where Trichinella would settle. “The only reason they went where they went was because of bile.”

Sukhdeo turned to his liver flukes, and he found that they also followed rules instead of gradients. Because they have a longer journey than Trichinella, they need three rules instead of two. When a liver cyst tumbles into the intestines, it’s sensitive to bile as well. When it senses it, it starts twitching—“it goes spastic,” says Sukhdeo. As it writhes, it breaks open its cyst, and the same movements drive it through the mushy wall of the intestines and into the abdominal cavity. A liver fluke has two suckers, one by its mouth and one by its belly. It can crawl by extending its front sucker, clamping it down, and then pulling up the rest of its body and anchoring it with the belly sucker. Flukes can also crimp—their whole body suddenly contracts in a violent spasm, and they let go of both suckers.

These kinds of movements are all that a fluke needs to get to the liver. It doesn’t need a copy of Gray’s Anatomy showing it the way. When it emerges out of the small intestines, it crimps itself out into the abdominal cavity, eventually reaching the smooth wall of abdominal muscles. The following day, the fluke switches to creeping. Now safe from the torrents of the intestines, it creeps along the abdominal wall without having to worry about getting washed away.

At this point, a creeping liver fluke will almost always reach the liver, no matter which way it travels. You might expect that the fluke at least has to know a few things: which way is up and which is down, for example, or the fact that the liver is next to the pancreas but not the gallbladder. Not so. The fluke takes advantage of the fact that the abdominal cavity is like the inside of a beach ball. Even if it crawls straight down to the bottom, it will reach the liver if it simply continues to crawl in a straight line, coming back around to the top, where the liver sits. That’s why Sukhdeo found that 95 percent of flukes enter the liver from its upper side where it meets the diaphragm—the summit of the abdominal cavity. Despite the fact that a liver’s underside is big and closer to the intestines, only 5 percent penetrate it from that side.

It took a decade for Sukhdeo to figure out how these two parasites navigate. These days he is almost respectable. To his surprise, he was offered a job as a parasitologist at Rutgers despite his years in limbo. He has a lab full of students eager to decipher the navigation of other parasites. He’s thinking of ways to turn his discoveries into a way to kill parasites by giving them navigation signals at the wrong time. And he has many more puzzles to work on. When I last spoke to Sukhdeo, he was working on another fluke. It also starts out in a snail, but when it emerges from this host, it seeks out a fish instead of a sheep. As the fish swims past, the fluke snags onto the fish’s tail and burrows into the meat. It then makes a beeline through the muscle for the fish’s head and comes to rest within the lens of the fish’s eye. “It seems that all the ideas people had before were wrong, so we’re starting from scratch,” he said.

Sukhdeo has earned the respect of other parasitologists for having shown that there is a behavior to parasites, that they make their way through the unique inner ecology of their hosts’ bodies, and that you can figure out the rules they obey. He even got an award not long ago for his work, a plaque that he hands to visitors with a puzzled look. “When they gave it to me, I said, ‘Why am I getting this?’ I had been blackballed for so many years.” There’s a note of nostalgia when he talks about being ignored and ridiculed. He once submitted a paper to a journal about animal behavior and was rejected. When he asked the editor why, the editor reread the paper and accepted it, saying, “I had no idea parasites behaved. Please excuse my vertebrate chauvinism.” And his old advisor wasn’t the only parasitologist to tell him he was making a mistake. “At a meeting I went to, I was saying that we had to use ecological concepts when we were looking at parasites, and I got this old parasitologist standing up and shouting ‘Heresy!’ with the spittle coming up. A heretic!”

The word made Sukhdeo smile, and at that moment his goatee looked particularly devilish. “It was the high point of my career.”

Once a parasite manages to find the place in its host where it will live, it can’t just sit back and enjoy life. For one thing, it needs a way to stay put in its new home. As an adult, a liver fluke is adapted only to life in the liver; put it in the heart or the lung and it will die. For every place that parasites have to live, evolution has produced a way for them to stay there. For example, there are parasitic copepods (a kind of crustacean) that live all over the bodies of fish. There are copepods that live in the eye of the Greenland shark. There are copepods that live on the scales of Mako sharks, and others that live on their gill arches. There are copepods that live inside the noses of blue sharks. There are copepods that ram themselves through the side of a swordfish and clamp onto its heart.

Each of these copepods looks so different from the other species that it’s hard for anyone except an expert to see that they all evolved from a common ancestor. Far from degenerating, these copepods have developed into bizarre forms in order to hold tight in their chosen niches. If these copepods should lose their grip, they would float away to a certain death. Every shark has its own special geometry of its scales, and copepods that live on the scales clasp their legs around them perfectly, like a lock and key. The copepod that lives in the Greenland shark has turned one of its legs into a mushroom-shaped anchor that it rams into the jelly of the eye.

Even for tapeworms, snug in the intestine, staying in place takes major effort. As they feed, tapeworms grow at a spectacular rate, increasing their size by a factor of as much as 1.8 million in two weeks. They can’t eat the way most animals do, because they have no mouth or gut. Their digestion doesn’t happen on the inside of their body but rather on the outside, their skin consisting of millions of delicate, blood-filled, fingery projections that can absorb food. The intestines of their host are also lined with almost identical projections. You could say that a tapeworm isn’t really missing a digestive tract—it’s an intestine turned inside out.

Tapeworms live in surging tides of half-digested food, blood, and bile, driven by the intestine’s endless peristalsis. If they do nothing, peristalsis will carry tapeworms out of their host altogether. Some species of tapeworms clamp themselves to the intestines with hooks and suckers on their heads, but others are perpetually slithering to where the food is. When we eat, peristalsis immediately ripples through our intestines, and these unanchored tapeworms respond by swimming upstream. They reach the incoming food and keep swimming until they hit the highest concentration. At that point, they soak up their meal through their skin, but as they eat, the food is carried downstream, and for a while the tapeworms let themselves be carried along with their movable feast. All the while, the tapeworms keep track of how far they’ve drifted by sensing how their host’s peristalsis changes. If they move too far downstream, they stop eating and swim back up. As tapeworms grow to their spectacular lengths, this swimming upstream can get to be complicated. The trouble is that peristalsis may make the intestines ripple quickly in one place and not at all farther up. Somehow tapeworms can detect these differences. They respond by making some parts of their body swim fast and some slowly.

The intestines are also home to hookworms, parasites that play a far riskier game whenever they eat. Hookworms start their lives in damp soil, where they hatch from eggs and grow into tiny larvae. They can travel into a human body by two routes: one simple, one tortuous. If a person swallows a larva, it will travel straight down to the intestines. But hookworms, like blood flukes, can penetrate the skin and burrow into a capillary. They swim through the veins to the heart and the lungs. When their host coughs, the larvae are carried up into their throat and can head down the esophagus.

Once it gets into the intestines, the hookworm grows into an adult, about half an inch long. Unlike tapeworms, the hookworm has a mouth—a powerful one ringed with daggerlike teeth and attached to a powerful, muscle-lined esophagus. And unlike tapeworms, it’s not interested in the half-digested food flowing through the intestines but in the intestines themselves. It drives it mouth into the lining of the intestines, ripping up the flesh. Parasitologists are still debating whether hookworms then drink their host’s blood or sop up the torn-up intestinal tissue. In either case, they release their grip after a while and swim to a new patch of tissue to feed.

But when the hookworm tears up some intestine and puts it in its mouth, the blood starts to clot. Whenever a blood vessel is torn, it picks up molecules from the cells in the surrounding tissue. Some of these new molecules combine with compounds floating in the blood itself. These chemicals trigger a cascade of reactions with other factors in the blood, which ultimately activate special cells known as platelets. The platelets swarm to the wound and clump together, while the cascade also creates a mesh of fibers around them, forming a hard clot that stops the bleeding. For a hookworm, clotting can mean starvation as the blood vessels in its mouth turn hard.

The parasite responds with a sophistication biotechnologists can only ape. It releases molecules of its own that are precisely shaped to combine with different factors in the clotting cascade. By neutralizing them, the hookworm keeps the platelets from clumping and allows the blood to keep flowing into its mouth. Once a hookworm finishes feeding at one place, the vessels can recover and clot while the parasite moves on to a fresh bit of intestines. If the hookworm were to use some crude blood-thinner that flooded the intestines, it would turn its hosts into hemophiliacs who would quickly bleed to death and take away the hookworm’s meal. A biotechnology company has isolated these molecules and is now trying to turn them into anticlotting drugs.

For some parasites, reaching their new home in the body is not enough. Before they can eat and multiply, they build new houses for themselves, using their host’s tissue as lumber.

Plasmodium, the parasite that causes malaria, enters the bloodstream through a mosquito bite and lives for a week or so in a liver cell. It then breaks out and gets back into the bloodstream. It rolls and yaws its way in search of its next home, a red blood cell. It’s here in the red blood cell that Plasmodium can feed on hemoglobin, the molecule that holds on to the oxygen that the red blood cells carry from the lungs. Devouring most of the hemoglobin in a cell, Plasmodium can gain enough energy to divide into sixteen new versions of itself, a flock of new parasites bursting out of the cell after two days, all searching the blood for new cells to invade.

Red blood cells are in many ways an awful place to live. Strictly speaking, they’re not even cells at all; they’re corpuscles. All true cells carry genes in a nucleus and duplicate their DNA in order to become two new cells. Red blood cells originate from cells deep inside our bones. These stem cells, as they’re known, divide and take the form of the various components of the blood, such as white blood cells, platelets, and red blood cells. But while other cells get their proper rations of DNA and proteins, red blood cells get no DNA at all. Their job is simple. In the lungs they store oxygen in molecules of hemoglobin. Because oxygen is a powerful atom that can easily react—and damage other molecules—the hemoglobin actually surrounds it by its four chains. Once the red blood cell leaves the lungs and travels through the body, it eventually sets the oxygen free to help the body burn its fuel to produce energy. The cells are simply crates pushed through the circulatory system by a beating heart. If you put white blood cells under a microscope, they reach out lobes to drag themselves across the slide. Red blood cells just sit on the glass.

Because their job is so simple, red blood cells don’t need much metabolism. That means they carry few of the necessary proteins for generating energy. Nor do they need to burn fuel and pump out waste. A true cell pumps its fuel in and spits its trash out by means of elaborate channels and bubbles that can shuttle molecules across its outer membrane. A red blood cell has hardly any of this equipment—a couple of channels for water and other essentials—because oxygen and carbon dioxide can diffuse through its membrane without any help. And while other cells have intricate scaffolding inside their membranes to keep them stiff and strong, a red blood cell is the contortionist of the body’s cellular circus. It travels three hundred miles in its lifetime, blasted and buffeted by the flow of blood, crashing into vessel walls and getting squeezed through slender capillaries, where it has to travel with other red blood cells in single file, compressed to about a fifth of its normal diameter, bouncing back to its normal size once it’s through.

In order to survive the abuse, the red blood cell has a network of proteins undergirding its membrane that are arrayed like the knit of a mesh bag. Each string of proteins making up the mesh is also folded up like a concertina, allowing it to stretch out and squeeze back in response to stress coming from any direction. But as flexible as a red blood cell may be, it can’t take this abuse forever. Over time its membrane becomes stiff, and it has a harder time squeezing through the capillaries. It’s the spleen’s job to keep the body’s blood supply young and vibrant. As red blood cells pass through the spleen it inspects them carefully. It can recognize the signs of old age on the surface of red blood cells, like the wrinkles on a face. Only young red blood cells make it out of the spleen; the rest are destroyed.

Despite all of the disadvantages of a red blood cell, Plasmodium seeks out this strange empty house. The parasites can’t swim, but they can glide along the walls of blood vessels. To do so, they set down hooks on the vessel wall, drag them back to their tail end, and put new hooks down to take their place, like a cellular tank tread. At the parasite’s tip are sensors that respond only to young red blood cells, clasping on to proteins on the cells’ surface. Once Plasmodium fixes on a cell, it latches on and rolls itself over onto its head and prepares to invade.

The head of the parasite is ringed by a set of chambers like the barrel of a revolver. Out of the chambers comes a blitz of molecules in a matter of seconds. Some of the molecules help the parasite push aside the membrane skeleton and work its way inside. The same hooks that acted as the parasite’s tank treads while it wandered along the vessel walls now latch on to the edges of the hole and drive the parasite through it. The parasite blasts out sheets of molecules, which join together and form a shroud around the parasite as it goes in. Fifteen seconds after the blast, Plasmodium’s back end disappears through the hole, and the resilient meshwork of the red blood cell simply bounces back again, sealing itself shut.

Once inside, the parasite is in the pantry. Each red blood cell’s interior is 95 percent hemoglobin. Plasmodium has a mouth of sorts on one side—a port that can swing open—and when it does, the outer membrane of the parasite’s bubble opens as well, bringing the parasite briefly into contact with the red blood cell’s contents. A little dollop of hemoglobin oozes into the maw, which then twists shut. The hemoglobin now floats in a bubble inside the parasite, which contains molecular scalpels that slice apart the molecules. Plasmodium makes a succession of cuts that open up their folded branches, letting them fall apart into smaller pieces and capturing the energy that had been held in those bonds. The core of hemoglobin molecules is a strongly charged, iron-rich compound that is poisonous to the parasite. It tends to lodge itself in Plasmodium’s membrane, where its charge disrupts the normal flow of other molecules in and out. But Plasmodium can neutralize the toxic heart of its meal. It strings some of it in a long, inert molecule called hemozoin. The rest of the compound gets processed by the parasite’s enzymes, which reduce its charge and make it unable to penetrate the membrane.

Plasmodium does not live by hemoglobin alone, however. It needs amino acids to build its molecular scalpels, and it also needs them to multiply into sixteen new copies. In those two days, the metabolic rate within an infected cell rises three hundred fifty times, and the parasite needs to make new proteins and get rid of the wastes that it makes as it grows. If Plasmodium had infected a true cell, it could simply hijack its host’s biochemistry for those jobs, but in a red blood cell it has to build the machinery from scratch. In other words, Plasmodium has to transform these mere corpuscles into proper cells. Out from its bubble it extends a tangled maze of tubes that reach all the way to the membrane of the red blood cell itself. It’s not clear whether Plasmodium’s tubes actually punch their way through the membrane of the red blood cell or jack into the channels that are already there. In either case, the parasitized red blood cell can start dragging in the building blocks the parasite needs to grow.

Suddenly crowded with channels and tubes, the surface of the red blood cell starts to lose its springiness. This could be fatal for the parasite, because if the spleen discovers that the cell is no longer its lithe young self, it will destroy it—along with any parasites it may harbor. As soon as it enters the red blood cell, Plasmodium releases proteins that are ferried through the tubes to the underside of the cell’s membrane. These molecules belong to a common class of proteins found in every sort of organism on Earth. Known as chaperones, they help other proteins fold and unfold properly even when they’re being disrupted by heat or acid. In the case of Plasmodium’s proteins, though, the chaperones seem to protect the red blood cell from the parasite itself. They help the cell’s skeleton stretch out and collapse back tight again, despite the parasitic construction getting in their way.

Within a few hours, the parasite has transformed and stiffened the red blood cell so much that there’s no hope in trying to disguise it as a healthy corpuscle. Now the parasite dispatches a new set of proteins to the surface of the cell. Some of them ball up in clumps under the cell’s surface, giving the membrane a goose-bumpy look.

Plasmodium then pierces the goose bumps with sticky molecules that can grab hold of receptors on the cells of the blood vessel walls. As these red blood cells stick to the vessel walls they drop out of the body’s circulation. Rather than trying to sneak through the slaughterhouse of the spleen, Plasmodium evades it altogether. Their red blood cells instead clump up in capillaries in the brain, the liver, and other organs. Plasmodium spends another day dividing, until the red blood cell is nothing more than a taut skin around the bulging bundle of parasites. Finally, the new generation of Plasmodium breaks out of the cell and looks for new red blood cells to invade. Left behind in the dead cell is a clump of used-up hemoglobin. For a time the cell was the parasite’s home, a cell like none other in the human body, but in the end it becomes its garbage dump.

Trichinella is also a biological renovator, and in some ways it’s more impressive than Plasmodium: it’s a multicellular animal that can live inside a single cell. When this worm hatches from an egg in its host’s gut, it drills through the intestinal wall and travels the body through the circulatory system. It follows the flow into the fine capillaries, where it leaves the bloodstream and works its way into the muscles. It crawls along the long muscle fibers and then penetrates one of the long, spindle-shaped cells that make them up. In the 1840s, when scientists first recognized Trichinella’s cysts lodged in muscles, they thought the tissue had degenerated and that the parasite slept inside, simply waiting to reach its final host. At first, the invaded muscle cell does seem to atrophy. The proteins that serve as the scaffolding of the cell and make it rigid fade away. The muscle’s own DNA loses its power to make new proteins, and within a few days after the worm has entered, the muscle changes from wiry to smooth and disorganized.

But the parasite is only tearing down the cell so that it can rebuild it. Trichinella doesn’t disable its host’s genes—in fact, they start copying themselves until they’ve quadrupled. But this abundance of genes now follows Trichinella’s commands, making proteins that will turn the cell into a proper home for the parasite. Scientists once thought this kind of genetic control was limited to viruses, which use their host’s DNA to make more copies of themselves. Trichinella, they now realize, is a viral animal.

Trichinella turns the muscle cell into a parasite placenta. By making the muscle cell loose and flexible, the parasite makes room on its surface for new receptors for taking in food. The parasite also forces the cell’s DNA to churn out collagen, which forms a tough capsule around the cell. It makes the cell produce a signal molecule known as vascular endothelial growth factor. This molecule normally sends a signal to blood vessels to grow new branches in order to help heal wounds or nurture growing tissues. Trichinella uses the signal for its own purposes: to weave a mesh of capillaries around it, using the collagen capsule as their mold. Through the vessels comes a nourishing flow of blood, allowing the parasite to grow and swell inside its muscle cell, which bulges and groans as the worm rocks back and forth and probes its little home.

Parasites can also reconstruct the interiors of plants as drastically as they can those of animals. It may come as a surprise that plants actually have parasites at all, but they’re positively overrun with them. Bacteria and viruses live happily in plants, sharing them with animals, fungi, and protozoa. (Trypanosomatids, close relatives of the parasites that give us sleeping sickness, can live inside palm trees.) Plants are even hosts to parasitic plants that drive their roots into their hosts. Parasitic plants come into this life lacking at least some of the skills that a plant needs to live on its own. Bird’s beak, which lives in salt marshes, is a part-time parasite that has to steal fresh water from pickleweed and other plants that can get rid of the salt; they can handle their own photosynthesis and get their own soil nutrients. Mistletoe can photosynthesize, but it can’t draw its own water and minerals from the soil. Broomrape can do nothing for itself.

There are also millions of species of insects and other animals that live on plants, but before 1980, few ecologists thought of them as parasites. They were considered herbivores, essentially little spineless goats. But Peter Price, an ecologist at Northern Arizona University, pointed out that there’s a fundamental difference between these animals and herbivores. Herbivores are to plants as predators are to prey: an animal that can eat any number of species. A coyote will be happy with a bat, a rabbit, or a cat, while a sheep is equally easy about the plants it eats, entering a field and devouring the clover, the timothy, the Queen Anne’s lace. Some insects, like woolly bear caterpillars, graze like sheep, taking small bites from individual plants of different species and moving on. But many insects are limited to only one plant, at least for one stage of their life. A caterpillar that goes from egg to pupa on a single milkweed plant is no different from a tapeworm, which can live as an adult only in the intestines of a human. And many plant-eating insects spend their entire lives on a single plant, shaping their lives to that of their host.

One of the most powerful demonstrations of Price’s argument is nematodes that live in plant roots. These parasites are spectacular pests, destroying 12 percent of all the cash crops in the world. One particular kind—root-knot nematodes of the genus Meloidogyne—are also an uncanny botanical reflection of Trichinella. Each nematode hatches from an egg in the soil and crawls to the tip of a root. It carries a hollow spike in its mouth, which it stabs into the root. Its saliva makes the outer cells burst, freeing up a space through which the nematode can slip. It nudges its way between the cells inside the root until it reaches the root’s core.

The nematode then pierces a few cells around it, injecting a peculiar poison into them. The cells start making copies of their DNA, and the extra gene starts making a flurry of proteins. Genes switch on in these root cells that would never normally become active. The job of a root cell is to pull in water and nutrients from the soil and pump them into a plant’s circulatory system, a network of tubes and cavities that carries the food to the rest of the plant. But under the spell of the nematode, a root cell starts working backward. It begins to suck in food from the plant. Its cell walls become leaky enough to let the food flow in easily, and it sprouts fingery ingrowths, where it can store the food. The nematode spits molecules into the altered cell, which form themselves into a sort of intercellular straw, which it uses to suck up the food being pumped in from the rest of the plant. As the cell swells with food, it threatens to burst the entire root open. To protect it, the nematode makes the surrounding cells multiply and form a sturdy root knot to withstand the pressure. Just as Trichinella speaks the genetic language of mammals, root nematodes have learned the language of plants.

Parasites live in a warped version of the outer world, a place with its own rules of navigation, of finding food and making a home. While a badger digs itself a den or a bird weaves itself a nest, parasites often act as architects, casting a biochemical spell to make flesh and blood change into the form they desire, a heap of planks swirling together into a house. And inside their hosts, parasites also have their own bizarre inner ecology.

Ecologists study how the millions of species on Earth share the world, but rather than take on the whole planet at once, they generally focus on a single ecosystem, be it a prairie, a tidal flat, or a sand dune. Even within those limits, they are frustrated by loose frontiers, by the way seeds blow in from miles away or wolves lope in from the other side of a mountain. As a result, ecologists have done some of their most important work on islands, which may be colonized only a few times over the course of millions of years. Islands are nature’s own isolated laboratories. On them, ecologists have figured out how the size of a given habitat determines how many species can survive on it. And they’ve taken that knowledge back to the mainland, showing how a fragmented ecosystem becomes its own archipelago, where extinctions can strike.

To a parasite, a host is a living island. Bigger hosts tend to have more species of parasites in them than small ones, just as Madagascar has more species than the Seychelles. But as islands go, hosts have some quirks. Parasites can find in them a vast number of ecological niches, because a body has so many different places to which they can adapt. On the gills of a single fish, a hundred different species of parasites may each find their own niche. An intestine may look like a simple cylinder, but to a parasite, each stretch has a unique combination of acidity, of oxygen levels, of food. A parasite may be designed for living on the surface of the intestines, inside the film that coats it, or deep among its fingerlike projections. In the bowels of a duck, fourteen species of parasitic worms may live (their combined population is on average twenty-two thousand), and each species takes as its home a particular stretch of intestine, sometimes overlapping with its neighbors, often not. Parasites can even find a way to parcel out the human eye: one species of worm in the retina, one in the chamber, one in the white of the eye, one in the orbit.

In hosts where parasites can find enough niches, they don’t compete over their island of flesh. But when they all want the same niche, ugliness usually breaks out. A dozen species of flukes may be able to infect a single snail, for example, but they all need to live in its digestive gland to survive. When parasitologists crack open the shells of snails, they typically don’t find those dozen species of flukes inside, but several individuals from one species. The flukes may devour their competition or release chemicals that make it harder for newcomers to invade. Other parasites living inside other animals can also compete with one another. When thorny-headed worms arrive in a rat’s intestines, they drive tapeworms out of the most fertile region, exiling them down into a stretch of the bowels where it’s much harder to find food.

The most vicious and unneighborly behavior of all, though, can be found among some of the parasitic wasps that so impressed Darwin. This shouldn’t come as too much of a surprise, given the gruesome way the wasps treat their hosts. The mother wasp roams over the countryside, sniffing the air for the scent of the plants its host—often a caterpillar but sometimes another insect such as an aphid or an ant—feeds on. Once it gets closer, it sniffs for the scent of the caterpillar itself or its droppings. Parasitic wasps alight on their host and jam their stinger into the soft section between the plates of the caterpillar’s exoskeleton. Their stinger isn’t actually a stinger at all, though; it is actually called an ovipositor, and it delivers eggs—in some cases just a handful, in others hundreds. Some wasps also inject venom that paralyzes their hosts, while others let them go back to feeding on leaves and stems. In either case, the wasp eggs hatch, and larvae emerge into the caterpillar’s body cavity. Some species only drink the caterpillar’s blood; others also dine on its flesh. The wasps keep their host alive for as long as they need to develop, sparing the vital organs. After a few days or weeks, the wasp larvae emerge from the caterpillar, plugging up their exit holes behind them and weaving themselves cocoons that stud the dying host. They mature into adult wasps and fly away, and only then does the caterpillar give up the entomological ghost.

When different species of wasps compete for the same caterpillar, it can become a brutal struggle. A clutch of wasp larvae may end up stunted and starved if they face too much competition, and the danger is worse for wasps that need a long time to mature in caterpillars. The wasp Copidosoma floridanum takes an entire month to mature inside the cabbage looper moth. As a result, it is a staggeringly unfriendly parasite.

Typically, Copidosoma lays only two eggs in its host, one male and one female. As with any egg, each begins as a single cell and divides, but then it veers away from the normal path of development most animals follow. The cluster of wasp cells divides itself up into hundreds of smaller clusters, each of which then develops into separate wasps. Suddenly, a single egg gives rise to twelve hundred clones. Some of the clusters develop much faster than the rest, becoming fully formed larvae only four days after their original egg was laid. These two hundred larvae, known as soldiers, are long and slender females, with tapered tails and sharp mandibles. They roam through the caterpillar, seeking out one of the tubes the caterpillar uses to breathe. They wrap their tails around a breathing tube, and like sea horses anchored to a coral reef, they rock in the flow of caterpillar blood.

The task for these soldiers is simple: they live only to kill other wasps. Any wasp larva that passes by, whether other Copidosoma floridanum or another species, prompts a soldier to lash out from its tube, snagging the larva in its mandibles, sucking out its guts, and letting the emptied corpse float away. As this slaughter goes on, the rest of the Copidosoma embryos slowly develop and finally grow into a thousand more wasp larvae. These larvae, called reproductives, look very different from the soldiers. They have only a siphon for a mouth, and they’re so tubby and sluggish that they can move only by being carried by the flow of the caterpillar’s blood. Reproductives would be helpless against any attack, but thanks to the soldiers, they can just drink the caterpillar’s juices as the shriveled corpses of their rivals float past.

After a while, the soldiers turn on their siblings—more specifically, on their brothers. A mother Copidosoma lays one male egg and one female egg; after they’ve both multiplied, they produce a fifty-fifty split betwen the sexes. But the soldiers selectively kill the males so that the vast majority of survivors are females. Entomologists once documented two thousand sisters and a single brother Copidosoma emerging from a caterpillar.

The soldiers turn on their own brothers for sensible evolutionary reasons. Males do nothing for their future offspring beyond providing sperm. Copidosoma’s hosts are hard to find—they are spread out like islands separated by miles of ocean, so males that emerge from a caterpillar will probably mate successfully close to home with their sisters. In such a situation, only a few males are necessary, and any more would mean fewer females for them to mate with, and fewer offspring. By killing the male reproductives, the female soldiers ensure that the host will be able to support the most females possible and help carry on the genes they share with their sisters.

As ruthless as soldiers may be, they’re also selfless. They are born without the equipment for escaping the caterpillar themselves. While their reproductive siblings drill out of the host and build themselves cocoons, the soldiers are trapped inside. When their host dies, they die with it.

Making that final journey—leaving the host—is the most important step in a parasite’s existence. It takes particular care to be ready to get out when the time is right, because otherwise it will be doomed to die with its host. That’s why people who need to be tested for elephantiasis, as Michael Sukhdeo was as a child, have to be tested at night. The adult filarial worms live in the lymph channels, and the baby worms they produce move into the bloodstream, spending most of their time in the capillaries in tissues deep within the body. But the only way for a baby worm to grow to adulthood is to be taken up in the bite of mosquitoes that come out at night. Somehow, deep inside our bodies, the worms can figure out what time of the day it is—perhaps by sensing the rise and fall of their host’s body temperature—and move out into the blood vessels just under the skin, where they’re likely to get sucked up by a mosquito. By two in the morning, the worms that haven’t been picked up in a bite start moving back to their host’s core to wait for the next dusk.

Parasites can also use hormones to signal them when it’s time to leave. The fleas on a female rabbit’s skin can detect hormones in the blood they drink from her. They can tell when she’s about to give birth, and they respond by rushing to the front of her face. Once she has delivered her babies and is nuzzling and licking them, the fleas leap onto the newborns. Baby rabbits can’t groom themselves yet, and their mothers clean them only when they visit their nest once a day to nurse. That makes the baby rabbits wonderfully tranquil homes for fleas. The fleas immediately start feeding on the babies, mating, and laying eggs. The new generation of fleas grows up on the babies, but when they sense that the mother is pregnant again, they hop back on her. There they wait to infect her next litter.

Getting to a new host can become a huge challenge when a parasite’s species of choice is a solitary creature. Dig a few feet down into the hard summer dirt of an Arizona desert, for example, and you may a find a toad. It is the spadefoot toad Scaphiopus couchi, and it is sleeping away the eleven-month drought that dominates every year. It sits underground, not eating, not drinking. Its heart barely beats, but its cells still have to purr metabolically along, and it stores its wastes in its liver and bladder. In July or August the first rains come, monsoons that roar down and break up the soil. On the first wet night the toads come alive and crawl out.

The toads gather in ponds, where the males outnumber the females ten to one. They attract the females by singing in floating choruses, croaking so passionately that their throats bleed. A female drifts among the males until she finds the voice she likes and nudges the male. He climbs on her and they lock together, the female letting slide a raft of eggs that the male fertilizes with his sperm. By four in the morning the courtship is over. Before the hot sun rises, the toads have crawled back down a few inches into the ground. Only when the sun sets again (and only if there’s enough water) will the toads return to the surface. When they aren’t mating, the toads are eating enough food to tide them over for the rest of the year. A toad can eat half its weight in termites in one night. Meanwhile, their offspring grow frantically from egg to toadlet in only ten days, since the rainy season is only a few weeks long. As the rains taper off the toads all disappear underground, having spent a few days out of the earth, and return to their life of sleep.

With so little opportunity to go from host to host, a spadefoot toad might seem a bad choice for a parasite. There are, in fact, hardly any parasites that have gotten a foothold inside the spadefoot, and most of them can only mount feeble infections. But one parasite positively revels in the spadefoot life, a worm named Pseudodiplorchis americanus. Pseudodiplorchis belongs to a group of parasites called monogeneans, delicate blobby worms that almost always live on the skin of fish and travel from host to host in the comfort of ever-present water. Yet, half of spadefoot toads carry the monogenean Pseudodiplorchis, and each toad carries an average of five.

Of all places, Pseudodiplorchis chooses the toad’s bladder to live during the long sleep. As the toad pumps more salts and other wastes into the bladder the parasite goes on with its life, sucking blood and mating. Within each female Pseudodiplorchis, hundreds of eggs mature into larvae. They sit inside her for months, waiting for the toad to rouse. The parasites will wait as long as the toad waits, even if the rains don’t come until the next year. When the rains do fall, the parasite is caught in a deluge of its own. After the toad has clawed its way to the ground, its skin soaks up water, which floods through its bloodstream, scouring out all the poisonous waste that has built up in its body over the year, through its kidneys and into its bladder. This torrent of urine suddenly turns the parasite’s habitat from a salty ocean to a freshwater pool. Pseudodiplorchis holds tight during the torrent and goes on waiting. It waits out the male choruses and the female inspections. Only when their toad host is sexually aroused as it tries to mate with another toad does a mother Pseudodiplorchis send her hundreds of young rushing out of the bladder and into the pond. When they reach the water, they rip out of their egg sacs and swim free.

Now, after their eleven-month wait, the parasites have to race. They have only a few hours to find another host in the mating pool before the toads crawl back underground and the sun rises and any stranded parasites fry. As they swim through the pond they have to be sure that they don’t crawl onto one of the other species of desert toads that crowd the water as well. Some kind of unique skin secretion from the spadefoot probably guides them to their host. Pseudodiplorchis has an awesome homing ability in its ponds. For many parasites, it’s not unusual for only a few out of thousands of larvae to find a host in which they can mature. Pseudodiplorchis has a success rate of 30 percent. As soon as it hits its host, a Pseudodiplorchis larva starts crawling up the toad’s side. It comes out of the water altogether, climbing as high as it can go. It ends up on the toad’s head, and once there, it can find the nostrils and slip inside.

The race goes on further: Pseudodiplorchis still has to get into the toad’s bladder before the rainy season ends. And within the toad, Pseudodiplorchis faces conditions just as murderous as the desert sun. It travels down the toad’s windpipe, drinking blood as it goes, until it gets to the lungs. There it lives for two weeks, fighting off the toad’s efforts to cough it up, maturing into a young adult about a tenth of an inch long. It leaves the lungs and crawls into the toad’s mouth, only to turn around and dive down its esophagus and into its gut.

The acids and enzymes the toad uses to digest its food should dissolve such a delicate parasite. If you pull a newly arrived Pseudodiplorchis out of a toad’s lung and stick it directly into its intestines, the parasite will die in minutes. But in its two weeks in the lungs, it can prepare itself for the trip by storing up a collection of liquid-filled bubbles in its skin. When it dives into the toad’s digestive tract, it lets the bubbles burst, spilling out chemicals that neutralize the compounds trying to digest it. Yet, even with this protection, Pseudodiplorchis doesn’t dawdle: it charges through the entire digestive tract of the toad in half an hour and makes its way into the bladder. The entire trip, from nose to lung to mouth to bladder, takes no more than three weeks, and by then the host toad has finished its annual mating and feasting and is back underground.

The spadefoot toad is one of the few hosts that leads a life as isolated as its parasites; together they spend a year in the ground waiting for the chance to see their kind again.

Parasites have colonized the most hostile habitats nature has to offer, evolving beautifully intricate adaptations in the process. In this respect, they’re no different from their free-living counterparts, much as that might horrify Lankester. And I haven’t even had room in this chapter to talk about the most remarkable adaptation that parasites have made: fighting off the attack of the immune system. That fight demands a chapter of its own.