A New Book on Parasites, Reviewed

A vacation in the Catskills, one of those beautiful summer days which seem to go on forever, with family friends down at a local pond. I must have been six. I waded around happily, in and out of the tall grasses that grew in the murky water, but when I emerged onto the shore my legs were studded with small black creatures. “Leeches! Don’t touch them!” my mother yelled. I stood terrified. My parents’ friends lit cigarettes and applied the glowing ends to the parasites, which exploded, showering me with blood.

Mom was right, up to a point. If you rip a leech off, you’ll probably leave its jaws behind in the skin, thereby heightening the risk of infection. But her friends’ remedy—back when people smoked, it was practically folk wisdom—isn’t advisable, either. A leech contains, in addition to your blood, plenty of things you don’t want in an open wound. There are ways to safely remove a leech, but almost any source you consult will also make a surprising suggestion: just leave it there. Once the creature has finished making a meal of you—in around twenty minutes—it will drop off, sated. In the meantime, the guest, however unwelcome, is likely doing you no harm. After all, treatment with leeches was a staple of medicine for millennia, and has even been resurgent in recent decades, in applications where the anticoagulant properties of leech saliva are beneficial.

Sensible advice, but why does it feel so wrong? Simply put, we are taught to think of parasites with revulsion. “They are seen as blood suckers, freeloaders, scroungers, flunkies, deadbeats, and the worst kind of groupies,” Scott Gardner, Judy Diamond, and Gabor Racz write in “Parasites” (Princeton), an approachable and often fascinating primer on the subject. The word “parasite,” as the authors note, comes from the Greek for “next to food”; what they don’t quite say is that it has always conveyed moral opprobrium. The biological meaning emerged only in the eighteenth century, in the wake of the scientific revolution. For ancient Greek and Roman satirists, the term denoted what many of us now assume to be the figurative meaning: a sponger, a schnorrer, a person dining at someone else’s table, at someone else’s expense. “Like rats we always eat other people’s food,” a shameless hanger-on says in one of Plautus’ comedies. Parasites, quite literally, have always had a bad name.

From my childhood right up through my medical training and beyond, the word carried a frightening resonance for me. In a course on parasitology, I got another look at leeches (now through a microscope) and also studied a variety of predatory worms. I learned that one of my favorite foods, gefilte fish, can, if inadequately cooked, harbor the tapeworm Diphyllobothrium latum. If the worm gets into the human gut, it interferes with the absorption of nutrients and can cause Vitamin B12 deficiency. During my internship, at Mass General, I evaluated a botanist who had recently returned from Africa with a fever of a hundred and four, shaking uncontrollably; looking through the microscope at his blood, I saw swarms of Plasmodia protists, the genus of single-cell parasite that causes malaria. In Boston in those days, a case like this was a rarity; there were lengthy discussions about the various strains of malaria, and how sickle-cell mutations could mitigate the disease. Sadly, my colleagues and I were to become far more familiar with life-threatening parasitic infections. In the early years of the AIDS epidemic, I lost many of my patients to them. An AIDS patient’s devastated immune system might allow the parasite Toxoplasma gondii, carried by cats, to form brain abscesses; Cryptosporidium infection, which normally infests cattle, caused wasting from relentless diarrhea.

Even when the victims aren’t people, there is something about parasites that arouses appalled fascination. The authors of “Parasite” mention the monster in the film “Alien” as a kind of archetype of the gross-outs in which the field abounds. There’s Cymothoa exigua, a louse that destroys fishes’ tongues and then lives in their mouths, performing a tongue’s functions while gorging itself. The fungus Ophiocordyceps unilateralis, which propagates itself by taking over ants’ bodies, has sufficient notoriety that it appears in the video game The Last of Us, where it zombifies people rather than ants.

By and large, Gardner, Diamond, and Racz resist filling their book with nightmarish creatures. As researchers at the University of Nebraska and its affiliated state museum, which has a large parasitological collection, they want to give us a new understanding of parasites, to counter our unalloyed horror and instill a more scientifically nuanced view. They do this by widening our focus, encouraging us to think in terms of ecosystems and evolutionary history. They write about how parasites may keep populations of species in balance, the ways in which they are imperilled by climate change, and what we owe them in terms of our understanding of genetics, organism development, and ancient human migrations. “Dependent relationships between different species are the norm among living organisms,” they write. “And these have evolved in every imaginable form.” The story the authors tell is one of coexistence, involving trade-offs for both parasite and host. (They mostly steer clear of parasitoids, parasites whose survival involves eventually killing their host.) Seen this way, parasitism emerges as no more or less appalling than the strategies adopted by so-called free-living species—predation, say, or grazing, or photosynthesis.

Few of us realize how ubiquitous parasites are in the earth’s ecosystem. “It has been said that every species of animal is either a parasite or a host,” the authors write. “Among all known animals, there are more species that live as parasites than are free-living.” Parasitic life styles exist in all major animal groups, with the single exception of echinoderms, the phylum containing starfish and sea urchins. Parasitism is rife, too, among plants and, as you’d expect, fungi. Many organisms are what are termed “obligate parasites,” unable to complete their life cycle in the absence of a host—and obligate parasites include viruses, which, some scientists contend, aren’t even alive until they hijack a host’s cells.

Among the parasitic infections that affect humans, a large portion are caused by various species of nematodes, a phylum of worms. Nematodes account for four-fifths of all animal species and are so plentiful that, the authors write, one could “line them up end to end and have nematodes in every meter across our entire galaxy.” Envisioning a “parasite Olympics,” the authors award their gold medal to the nematode Ascaris lumbricoides, which has succeeded in establishing residence in the intestines of a sixth of the human population, more than a billion people. The worm causes a tropical disease, ascariasis, whose symptoms include fever, abdominal pain, cough, vomiting, and weight loss. The success of the species comes in part from the fact that, unusually for a parasite, it doesn’t require an intermediate host—the way that malaria, say, needs a mosquito in order to infect a human. Instead, Ascaris is transmitted from person to person via contaminated feces. (Throughout the book, illustrations by Brenda Lee manage to portray such life cycles clearly without being too extravagantly disgusting, and the authors highlight the importance of “access to shoes, clean water, and adequate sanitation” in fighting nematode diseases.)

Once inside a human host, the adult female Ascaris produces some two hundred thousand eggs a day, each of which can survive for decades. Though the eggs are microscopic, the authors point out that the eggs produced in a single host in the course of a year weigh roughly the same as two sugar cubes. Multiplying this by the number of infected people worldwide, they calculate an astonishing biomass of sixty-six million kilograms—equivalent to that of eight thousand adult male elephants or three hundred and fifty adult blue whales. When a person experiences an Ascaris infection, eggs travel from the intestine and into the blood, the liver, the heart, and the lungs, penetrating the trachea, through which they are swallowed, ending up back in the gut. There they mature into worms a foot long, which mate and produce more eggs.

Another star in the human-parasite Olympics is the whipworm, Trichuris trichiura, which can cause gastrointestinal disorders, impaired growth, and abnormal cognitive development. It earns a medal not only because of its prevalence—there are more than two million cases in the southeastern United States alone—but also because of its long history of infecting people. After the frozen body of a Neolithic man known as Ötzi was found in the Alps, in 1991, it was discovered that when he was killed by a flint arrowhead, more than five thousand years ago, he was suffering from a whipworm infection.

“I do some of my best thinking while keeping you up.”

Cartoon by P. C. Vey

Even parasites that don’t infect people can harm us. In Ireland in the eighteen-forties, a potato blight caused by the parasitic pathogen Phytophthora infestans resulted in a famine that killed around a million people and led nearly two million more to emigrate. The fungus is thought to have originated in the Americas and to have been brought to Europe on ships, and the happenstance of this path of infection leads the authors to sound a note of caution: “Modern agriculture, in which each individual food plant is genetically identical to the next one in the row, is highly vulnerable to the worst effects of parasitic fungi.”

Why aren’t our bodies better at combatting parasites? The answer has to do with adaptation. Nematodes, for instance, have evolved to outwit our immune system, switching off inflammation that would otherwise purge them. They produce molecules that make the parasites invisible to our immune surveillance. For the authors, the wonder of parasite adaptation is perhaps best illustrated by the tapeworm, of which about twenty thousand species are known. Many have suckers at the front end, to attach to the bowel of the host; some have hooks that can be engaged or released depending on whether the worm needs to move with or against the peristaltic flow of the intestine itself. But the tapeworm’s true “superpower” is its long, flat body, which is made up of a chain of reproductive segments. The result is a parasite that, as the authors put it, is both “inventively self-contained and massively reproductive.” The tapeworm is essentially modular, able to break itself into “thousands of little packages, each containing up to hundreds of thousands of eggs.” This inherent flexibility has enabled tapeworms to adapt to a huge variety of hosts. Some tapeworms are “tiny stubs no more than a millimeter in length”; others, such as those that infect blue whales, can grow to more than a hundred feet.

In one of their more fanciful passages, the authors imagine a whale’s infection through the eyes of Jonah, who, according to the Hebrew Bible, was swallowed by a “big fish,” interpreted in recent centuries as a whale. The experience would have been far from solitary, apparently: “The first creatures that Jonah met in the whale’s gut would have been tens of thousands of relatively small nematode worms. Later on, he might have come across the 30 meter tapeworm known as Tetragonoporus calyptocephalus.” The fact that it’s impossible to imagine a human surviving in such conditions is the point, of course: tapeworms, which need very little oxygen, are beautifully adapted to their ecological niche. Jonah was lucky to have been spat out after three days, but any tapeworm could have happily spent its whole life inside the whale. Indeed, the authors note, tapeworms have no internal limits on their life span: they can live for as long as their host is alive.

The adaptability of parasites is only part of the story, however. After all, we, too, evolve, and mutations in our DNA can provide resistance to some pathogens. But such adaptations can entail costs as well as benefits. The plasmodia that cause malaria have been attacking our red blood cells for millennia, and some people have developed genetic mutations that confer some resistance. Unfortunately, these mutations are also associated with a couple of blood-cell disorders—sickle-cell disease and thalassemia. Resistance to malaria, in other words, appears to come at the price of having blood that is less able to carry oxygen.

Another example is the parasite Trypanosoma brucei, which causes the disease African trypanosomiasis, commonly known as sleeping sickness. This protist, as the authors mention, is transmitted to people via the bite of the tsetse fly; unless treated, it will fatally overwhelm the central nervous system. Down the hall from my office is the laboratory of Martin Pollak, one of the scientists whose work has led to a startling discovery related to this parasite. Some people of African descent appear to have developed resistance to sleeping sickness, because of variants in the gene APOL1, one of several genes that govern innate immunity. Again, there’s a cost. Pollak and his colleagues have found that the APOL1 variants correlated with an increased risk for high blood pressure and certain types of kidney disease. In the parts of sub-Saharan Africa most prone to sleeping sickness, this genetic trade-off could be worthwhile. But the disease is not endemic anywhere outside Africa, which means that some members of the African diaspora may now pay dearly for an immunity that they no longer need.

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