Another species of fluke can be found in the meadows of Europe and Asia, along with a few in North America and Australia. Known as Dicrocoelium dendriticum, or the lancet fluke, it makes cows and other grazers its host as an adult, and the cows spread their eggs in their manure. Hungry snails swallow the eggs, which hatch in their intestines. They drill through the wall of a snail’s gut and settle in the digestive gland. There the flukes produce a generation of cercariae, which make their way to the snail’s surface. The snail tries to defend itself from the parasites by blocking them off with walls of slime. The slime balls up around the cercariae, which the snail coughs up and leaves behind in the grass.
Next, along comes an ant. To an ant, a slime ball is positively delicious. Along with the slime, the ant may also swallow hundreds of lancet flukes as well. The parasites slide down into its gut, and they then wander for a while through its body, eventually moving to the cluster of nerves that control the ant’s mandibles. The parasites all travel together on this trip, but after visiting the nerves, they split up. Most of the lancet flukes head back to the abdomen, where they form cysts, but one or two stay behind in the ant’s head.
There they do some parasitic voodoo on their hosts. As the evening approaches and the air cools, the ants find themselves drawn away from their fellow ants on the ground and upward to the top of a blade of grass. Like flies infected with a fungus, the ants clamp down on the tip of the grass. But the lancet fluke has a different goal than the fungus does. The fungus uses its host as a catapult to shower its spores on other insects. The lancet fluke can continue to live only if it can get inside its final host, a mammal. Clamped to the tip of a grass blade, the infected ant is likely to be devoured by a cow or some other grazer passing by. When the ant tumbles into the cow’s stomach, the flukes burst out and make their way to the cow’s liver, where the flukes will live as adults.
But the lancet fluke, like the fungus, is very aware of the passing of time. If the ant sits the whole night without being eaten and the sun rises, the fluke lets the ant loosen its grip on the grass. The ant scurries back down to the ground and spends the day acting like a regular insect again. If the host were to bake in the heat of the direct sun, the parasite would die with it. When evening comes again, it sends the ant back up a blade of grass for another try.
Most parasites rarely try this sort of thing on humans, but a few do it very well. The guinea worm spends its early life curled up inside a copepod swimming in water. A person drinking that water swallows the copepod, and when it dissolves away in stomach acid, the guinea worm escapes. It slips into the intestines and burrows out into the abdominal cavity. From there it wanders through the connective tissue until it finds a mate. The two-inch male and the two-foot female have sex, and then the male looks for a place to die. The female slithers through the skin until she reaches a leg. As she travels, her fertilized eggs begin to develop, and by the time she has reached her destination the eggs have hatched and become a crowd of bustling juveniles in her uterus.
These juveniles need to get into a copepod if they are to become adults themselves, and so they drive their human host to water. They press against their mother’s uterus so hard that they force it partially out of her body, letting some of the larvae spill out. Adult guinea worms tame the human immune system so that they can travel through our bodies unharmed, but the juveniles do just the opposite. They draw a quick reaction that brings immune cells rushing to them, making the skin around them swell and blister. The easiest way for a victim to get some relief from the hot pain of the wound is to pour cool water on it or just stick the leg in a pond. The juveniles that have already escaped their mother inside the blister respond to the splash by swimming free. The mother responds to the water as well by getting rid of more of her young. She doesn’t herniate herself the way she did before; this time she lets her babies escape through an even stranger route: her mouth. For every splash, half a million baby guinea worms come heaving up through her esophagous. The contractions pull her out of the wound bit by bit until she and her young have all left the host—the mother to die, the young to search the water for a new copepod to curl up inside.
This manipulation works best when humans and copepods all depend on scarce supplies of water, because that makes it more likely a person will dump guinea worm larvae where their next host can be found. Not surprisingly, dracunculiasis, the disease caused by the guinea worm, is particularly bad in deserts, where people crowd around oases.
The guinea worm is the sort of parasite that is content to sit in its first host until it is accidentally swallowed by its next one. Other parasites don’t rely so much on luck. Their hosts come into regular contact, usually to eat or be eaten. Biting insects seek out humans and other vertebrates and drink their blood, and they are—not coincidentally—filled with parasites trying to get into us. Malaria and filariasis are spread by mosquitoes, sleeping sickness by tsetse flies, kala-azar by sand flies, river blindness by black flies. (Bacteria and viruses come along for the ride as well, spreading bubonic plague, dengue fever, and other diseases.) These parasites swim into the wound made by the insect and then live in our skin or bloodstream, where they are likely to be taken in the bite of the next passing insect. But simply being in the right place is not enough for many of them—they change the behavior of the insects to make them spread the parasites faster.
Drinking blood is not easy. When a mosquito lands on your arm, it has to drive its proboscis through the tough outer layers of your skin and then snake it around for a while to find a blood vessel. The longer it takes, the better its chances of getting slapped and being reduced to a bloody smear. And once the mosquito hits blood, your body responds by clotting the wound. Platelets swarm around the mosquito’s proboscis, releasing chemicals that make them form sticky clumps and attract other platelets. As the mosquito tries to drink, its smooth cocktail of blood turns into a thick milk shake. To buy themselves more time, mosquitoes put chemicals in their saliva that fight against the clotting. One of them, apyrase, cuts apart the glue made by the platelets; other chemicals widen blood vessels to bring in more blood.
The risks of drinking blood make mosquitoes afraid of commitment. If they find it too difficult to draw blood from a host, they’ll quickly fly to a new patch of skin. But if that host has malaria, the parasites inside will make him more attractive. Malaria interferes with the platelets of its host, making them do a bad job of clotting. When a mosquito hits blood in a person with malaria, it will find it easier to drink and will be more likely to suck it up, and the parasite along with it.
Once it gets into a mosquito, Plasmodium needs time before it can travel into another human. It needs to move into the mosquito’s gut, mate with other Plasmodium parasites, and reproduce. More than ten thousand ookinetes are formed this way in ten days. They develop into sporozoites that migrate up to the salivary gland, where they’re finally ready to enter a human. But up to that point, it doesn’t do the parasite any good for the mosquito to eat. The risks of getting squashed in midbite are offset by no benefit. So Plasmodium does its best to discourage its host from eating. A mosquito with ookinetes in it will give up trying to take a blood meal more easily than a parasite-free one.