I’m tailing a Ford pickup truck along the eastern bank of the Connecticut River. When we reach a sign for Lord Creek Farm, the pickup turns off the road and I follow up a dusty driveway. We park in the shadow of an enormous red horse barn, next to paddocks full of jump gates, where riding lessons are under way. Williams, a Biologist is driving the pickup.
We drive across the farm, past freshly groomed meadows, and into the forest. The morning is magnificent, the sunlight slipping through gaps in the canopy. But we’re not here to admire the scenery. We’re here on a hunt, and our quarry is the black-legged tick. If you want to find black-legged ticks, you could not ask for a more spectacularly infested piece of land than Lord Creek Farm.
“You get absolutely astronomical abundance here—maybe 1,000 ticks an acre,” Williams declares. He sounds both appalled and delighted.
Lord Creek Farm holds another attraction for Williams: it is located in the town of Lyme. As in Lyme disease, caused by bacteria known as Borrelia burgdorferi. As in the town where Lyme disease was first discovered in the late 1970s, before it was recognized across the United States, from New York to California. Today, a quarter of a century after its discovery, Lyme, Connecticut, is still a great place to study Lyme disease. Seventy percent of the ticks on Lord Creek Farm are infected with Borrelia. I’m hoping one of them doesn’t find me today.
Williams climbs out of the truck and grab blue plastic crates from the back. I follow Williams into the woods, walking over jewelweed, wine raspberries, and Japanese barberry, which stabs our legs with hypodermic thorns.
Barberry was brought to the United States in the late 1800s as an ornamental plant, and it has swept across the forests of 32 states. The plant grows into a man-size umbrella. Its branches dip down to the ground and begin to lay new roots, which become plants of their own. Williams and his colleagues have found that Japanese barberry also creates the humid conditions that let ticks thrive.
“It’s really depressing,” says Williams, looking down the slope. “The earth curves, and you still see barberry.”
Williams and I wade toward a tree tied with a blue ribbon. Nearby is a low orange flag, next to which is a gray metal Sherman live trap. Williams picks up the trap and tips in the door. No one’s inside. He walks to the next flag.
That trap is also empty. It takes four visits before he finally says, “Aha!” He tips the trap toward me, holding the door open. A white-footed mouse huddles at the base, calculating its best option for escape.
After checking 60 traps, Williams, Short, and Floyd emerge from the forest. Between them they’ve gathered eight mice—a low number, Williams notes. He sets his blue crate on the truck bed and pulls out three white plastic folding chairs. Short and Floyd bring out a plastic table and snap open its legs. It looks as if they’re going to have a picnic, but the equipment they put on the table dispels the impression: a box of syringes, a bottle of isoflurane, blue plastic gloves. They’re actually going to perform a surgery of sorts.
“You might get to see us do some mouse CPR,” says Williams.
He turns to Short. “I’ll do data,” he says. “You want to be in the hot seat?”
“I’ll be in the hot seat,” says Short.
Short sits down next to the crate of traps, soaks a cotton ball in isoflurane, and drops it in a ziplock bag. Tipping open a trap, he pulls out a mouse by the tail and slips it into the bag. The mouse scrambles around until the isoflurane vapors knock it out. In a few seconds it is asleep, its lungs rising and falling gently. Short pulls the mouse back out by the scruff of the neck and gets to work.
“Mice go out quickly and come back quickly,” says Williams. “That gives you a two-minute window.”
The first thing Short does is bring the mouse close to his nose so he can inspect its ears. “Two ticks,” he announces, holding the mouse out to Williams.
Williams takes a close look for himself. “One larva, one nymph,” he says.
The larva is a wisp of an animal about the size of a grain of salt, hatched within the past few weeks. Once a tick larva emerges from its egg, it immediately begins searching for a host. Scientists call this behavior questing, although a questing black-legged tick doesn’t have a lot in common with Sir Galahad. It just finds a good place to wait—on a stem of jewelweed, say, or a branch of barberry—in the hope of snagging onto a passing mammal.
The mouse that Williams holds picked up its questing tick larva on a walk through the woods. Once the tick larva recognized it had attached to a host, it crawled onto the mouse’s fur, made its way to an ear, where blood vessels run close to the skin, and began to drink blood.
A larva will drink for a few days, fall off, molt, and grow to be about twice as big. This next stage is known as the nymph stage.
The nymph that was clamped onto our mouse’s ear likely hatched a year ago and, after its larval meal, dropped off and survived the winter. In the summer, it reemerged to find a new host. Now it’s having the second meal of its life. Once it has finished feasting for a few days, it will drop off, molt, and become an adult. The adults quest once more for a host, but the males also search for a mate. After a female tick mates, it lays a few thousand eggs on the forest floor. Males and females both have a two-year life span.
There’s a fair chance that the nymph on this mouse’s ear is carrying Borrelia, which it is injecting into the mouse’s bloodstream. Ticks are born free of Borrelia; the larva on Short’s mouse may well be getting infected at this very moment. For Borrelia, mice are a bridge from one tick to another.
Short needs some blood from the animal, but its rodent vessels are too small to get a draw. He will have to go for the heart. He flips the mouse on its back and feels for its sternum. With a free hand, he picks up a thin syringe and guides the needle upward underneath the rib cage. In one smooth motion, the needle plunges into the mouse’s beating heart. After a moment, a few drops of blood flow into the syringe.
“It’s a lot easier with a deer,” says Williams. “You go for the jugular, and it’s like a hose of blood. With the mice, if you don’t go straight in and straight out, you’ll scramble their insides.”
Short pulls the syringe out, leaving the mouse no worse for wear. He hands the syringe to Floyd, weighs the mouse on a hanging scale—17 grams—and punches a metal tag into its ear. Short finishes up just as the mouse starts to wiggle awake. It’s still getting its bearing as he drops it back into its Sherman trap and lets the door snap shut. (He’ll release it later.) Floyd transfers the mouse’s blood into an ampoule, which she puts into a baby blue Igloo cooler sitting by her feet.
When Floyd, Short, and Williams get back to New Haven this afternoon, they’ll hand the cooler over to a serologist, who will examine the eight blood samples for signs of antibodies. The mouse Short just impaled may turn out to be carrying Borrelia. And it may also be carrying other microbes that can make us sick. It may even carry pathogens that are entirely new to science. Ticks are champions at spreading diseases, expanding in both poor countries and rich ones, and delivering an extraordinary menagerie of bacteria, protozoans, and viruses. In a 2010 report on the dangers of ticks, the Institute of Medicine, the health arm of the National Academy of Sciences, declared the animals, with what sounds almost like admiration, “the Swiss Army knife of disease vectors.”
IT’S STARTLING to look at the graphs of tick-borne diseases over the past few decades. They’re mostly going in the wrong direction. The research on Lyme disease is fairly recent, sparked in the mid-1970s after a cluster of children around Lyme developed fever and aches. They were diagnosed with juvenile arthritis—a peculiar diagnosis for so many children in one place. Their parents searched for an explanation, and eventually Allan Steere, a doctor at Yale, figured out that they suffered from an infectious disease. The fact that they all came from a rural part of the state suggested that an insect or some other animal had delivered the infection. In 1982, Willy Burgdorfer, an entomologist with the National Institute of Allergy and Infectious Diseases, discovered corkscrew-shaped bacteria in black-legged ticks from Long Island. He exposed the bacteria to serum from people with Lyme disease and discovered that their antibodies swarmed around the microbes. That was a sign that these bacteria—which would later be named Borrelia burgdorferi after him—were the cause of Lyme disease.
Since Burgdorfer’s discovery, Lyme disease has spread relentlessly. New York and other northeastern states started recording new infections in the eighties. In the Midwest, Lyme disease came to light around the same time in Wisconsin and began radiating out from there. Today it can be found as far west as California, as far south as Virginia, and to the north across the border into Canada. Each year, 38,000 people in the United States are diagnosed with the condition. The list of symptoms includes fever, aches, fatigue, and, if left untreated for a length of time, arthritis, heart arrhythmia, and neurological damage. Lyme disease is rarely fatal.
While Lyme may be the best-known disease carried by ticks, it’s hardly the only one. In 1893, for example, veterinarians discovered that ticks harbored an amoeba-like pathogen that killed cows by the thousands. Babesia, as it came to be known, can also make people sick; the first case of human babesiosis was recorded in 1957 in Yugoslavia. Babesiosis causes a lot of the same symptoms as Lyme disease, such as fever, fatigue, and aches, as well as plenty of its own—like drenching sweats, nausea, and anemia.
Cases of babesiosis have been on the rise, following the same geographic pattern that Lyme did in the 1980s. The Centers for Disease Control and Prevention (CDC) started tracking babesiosis in 2011 and has since recorded 847 confirmed cases, along with 277 probable cases.
Both Babesia and Borrelia can be carried by the same black-legged tick, which means that a single bite can give you both. In fact, black-legged ticks can carry at least half a dozen pathogens, and that list is growing. In a January 2013 report, Yale scientists linked another species, Borrelia miyamotoi, to New Englanders sick with virus-like symptoms. They estimate that 4,000 Americans will be infected with it this year.
Other species of ticks in the United States carry their own menagerie of pathogens and havoc-wreaking proteins. The lone star tick, which lives in the Southeast and the Midwest, carries bacteria called Ehrlichia. Infection with Ehrlichia is rarely fatal, but the pathogen can cause fevers and aches and even kidney and lung damage. The lone star tick’s saliva also contains a protein that, injected into a person, can trigger a violent allergy to meat. Meanwhile, dog ticks and Rocky Mountain spotted ticks carry proteins that can, on rare occasion, cause a condition called tick paralysis. A victim’s legs start to go limp, and then the paralysis rises like a tide over the next few days. The cure is amazingly simple: remove the tick and the saliva runs out. Within an hour, a person will start to recover. But if it doesn’t occur to anyone to look for the tick, the tide of paralysis will keep rising.
The speech slurs, the breathing shallows, and the victim dies.
Ticks have been around for about 300 million years, according to evolutionary biologists, and today there are 878 known species, found on every continent. If you travel to Antarctica and walk along its coasts, you will find seabird ticks, Ixodes uriae, waiting on the frigid stones to attack any penguin that comes waddling by.
Tick species differ in size, shape, and color. Some are drab, while others have beautiful braided patterns of white and black on their backs. But in the all-important matter of getting a meal, they’re pretty much the same. A questing tick will find a good place to wait for a host. Many species have no eyes, but they can monitor vibrations in the ground and sense body heat, smells, and wafts of carbon dioxide. When a promising animal passes by, a tick reaches out with its legs, which have little hooks to grab hold.
Once a tick finds a host, it creeps along until it finds a good patch of skin to dig into—typically a place where the blood vessels run close to the surface and where it’s hard to be scratched away. It latches on with two of its legs, angles its back end in the air, and cuts open the skin with a mouth that looks like a Sawzall. Into the wound the tick inserts its barbed, tube-shaped mouthpart. The barbs make it hard for the tick to be removed; certain tick species lock themselves in place even more effectively by squirting out liquid cement, which forms a hardened cone around its mouthpart.
The shredded capillaries in its host’s skin gush out blood, forming a tiny subterranean pool. The tick draws up this blood slowly. One slurp may last as long as 20 minutes. After each drink, the tick reverses the flow and squirts saliva into the wound.
Tick saliva is an invertebrate magic potion. Normally, our body would quickly harden the blood pool with clots, but the tick’s saliva contains a protein that coaxes our own bodies to slice those clots apart. Other saliva proteins command the torn blood vessels to stay open wide to allow fresh blood to pour into the pool. Still others fend off the immune system and prevent us from feeling itchy.
Over the course of a few days, a feeding tick cycles between drinking and drooling. Its body swells. From larva to fully engorged adult, a female tick will grow to 2,880 times its original size. Try to imagine a human baby ballooning to the size of a small humpback whale—by eating only three meals over the course of two years. Such is the life of a tick.
Once a tick has had its fill, it dissolves its cement cone, pulls its mouthpart out of its host, and falls to the ground. While ticks may be best known as bloodsuckers, they spend most of their lives as starvers. Dehydration becomes a huge threat to their survival; many ticks desiccate before reaching the next stage in their life cycle. To keep from dehydrating, ticks will hide in humid spots on the forest floor. They also produce a spongy material that they gather around their mouthparts to absorb water from the air. Blizzards are a blessing to ticks; the snow insulates them from the cold air and can freeze-dry them into a state of suspended animation for weeks.
It’s a pretty grim existence, but as an evolutionary strategy it shows no signs of going out of style.
WILLIAMS HAS CONTRACTED Lyme disease at least three times over the course of his career. “It takes my wife to tell me,” he says. The symptoms come on quietly, disconnected. “If I get a knee ache, I take some Tylenol. I get grumpy. I get a fever at night,” says Williams. “She’s the one who says, ‘You’ve got Lyme.’” He has a month’s worth of antibiotics on standby.
Each time a tick saws into Williams’s skin, it may also unload microbes. Borrelia burgdorferi dwell in the guts of ticks. As soon as the tick takes in its first drop of blood, the corkscrew-shaped bacteria begin multiplying, slowly drilling their way out of the tick’s gut and through its body until they reach the salivary glands. (Their long journey means that if you carefully pull off a black-legged tick within 24 hours of getting bitten, you’ll almost certainly avoid getting Lyme disease.)
When the tick switches from drinking blood to spraying saliva, the bacteria travel from the blood pool into the torn capillaries surrounding the wound. From there they can spread through Williams’s bloodstream. The bacteria pick up Williams’s own enzymes along the way, using them to cut their way out of the blood vessels and into the surrounding tissues—be it cartilage around a knee or the muscle of the heart. Borrelia fuels its journey with the sugar floating through Williams’s body and hijacks his amino acids to build its own proteins.
Along the way, Borrelia also makes Williams sick. The bacteria don’t directly harm him—they inject no toxins into his cells—but they lead his immune system on a devastating chase. Some immune cells fight disease by engulfing invaders, like the Blob. Borrelia is so fast that it can outswim these monsters. Other immune cells gather intelligence to kill Borrelia, grabbing proteins and bringing them to the lymph nodes, where they manufacture new immune cells targeted to Borrelia.
But Borrelia can outfox these special forces, too. Some of the immune cells make antibodies that grab onto Borrelia and act as a beacon for other cells. The bacteria produces proteins of its own that destroy these antibodies first. To escape immune cells that recognize Borrelia by their surface proteins, Borrelia shucks off their old surface proteins and builds new ones, like a fugitive changing his wig and coat. The assassin cells, still relying on their obsolete profile of Borrelia, search for the bacteria in vain.
Our immune system produces inflammation as it chases after Borrelia, which causes the symptoms of Lyme disease. It’s that inflammation that is responsible for the telltale pink bull’s-eye on the skin around the bite, as well as the fevers and aches. If the disease isn’t caught soon enough, the inflammation can spread to the joints, causing severe pain and arthritis; to the heart, causing rhythm abnormalities; and to the brain, causing neurological damage and memory disorders.
The sooner Lyme disease is diagnosed, the more likely antibiotics can deliver a clean kill to Borrelia and stop the symptoms. Steven Kotler, a 46-year-old journalist and Outside contributor in Chimayo, New Mexico, knows all too well what happens when the bacteria go unnoticed for a length of time. The first sign that he had Lyme disease came in 1999, as he was driving from San Francisco to Los Angeles, where he was living at the time. “My left thigh cramped up so much I had to pull over,” he recalls. His life spiraled down from there; he began losing weight—eventually dropping 50 pounds—and ended up spending almost his entire day on the couch, too exhausted and in too much pain to get up. “I was crippled,” Kotler says.
Kotler had traveled to Madagascar the year before, so his doctors searched for worms and other parasites in his stool. They found none. In his 2006 book West of Jesus, he listed some of the diseases he was informed he had—including the flu, schizophrenia, lupus, leukemia, and strep throat. When Kotler heard about Lyme disease, which had not yet become familiar in California, he suggested it as a possibility to one of his doctors. After all, he had come down with his symptoms not long after he had gone to Long Island for a wedding. Perhaps he’d been bitten by a tick. “You don’t have Lyme,” his doctor told him. “You have AIDS.”
It took a year for Kotler to get properly diagnosed, and he was placed on antibiotics for months.
Afterward, many of the symptoms continued to plague him, including intense fatigue and a sometimes uncontrollable mood. It wasn’t until 2011 that Kotler felt back in the neighborhood of normal. Still, the damage had been done. “If I met you before I got Lyme, there’s a chance I won’t remember you,” he says.
IT’S HARD TO appreciate just how many ticks are out there. We usually encounter them one at a time, worriedly plucking lone individuals off our skin. The best way to reckon with the sheer number of ticks is to do what tick scientists do many times a year: go into the woods and perform a tick drag.
I did my first tick drag last fall in a forest just outside Millbrook, New York. My mentor was Andrea Goth, 26, at the time a project leader at the Cary Institute for Ecosystem Studies. She handed me a one-meter-square piece of cream-colored wide-wale corduroy. She had looped one end of the cloth over a wooden rod, which had a rope tied to each end. I laid the cloth flat on the forest floor and used the rope to pull it in a straight line for 100 meters.
When I got to the end of the transect, I wrapped a bungee cord around a young tree and hung the tick drag at shoulder height. It took a while to distinguish between black-legged tick larvae and bits of dirt. Pro tip: dirt doesn’t crawl.
Once you can see tick larvae, the cloth starts to swarm with them. I began grabbing the larvae with fine tweezers, the pressure of my fingers pushing their legs out to the side. I dumped each one into a tiny alcohol vial.
“I’m up to 28!” I called out. Goth was standing a few trees away, systematically plucking off larvae and nymphs from her own tick drag.
“Be glad it’s not 280,” she replied, not taking her eyes off her collection of ticks.
The sheer volume of black-legged ticks in the eastern United States is staggering, but it’s even more mind-blowing when you consider their history. Up until the mid-1900s, biologists found them only at the eastern end of Long Island and a few islands off the coast of Massachusetts.
Ticks themselves are awful travelers. During the months that they spend living on the ground, they may move a few yards. But when ticks climb aboard a host, they can travel for miles—especially on the deer that the adult ticks prefer.
Many experts think it’s no coincidence that black-legged ticks and deer have similar histories of expansion. During the 19th century, white-tailed deer nearly disappeared from the eastern United States as farmers plowed under most of their forests. In Connecticut, the population dropped down to a dozen or so animals in the entire state. “It was big news if someone saw a deer,” says Kirby Stafford, chief entomologist at the Connecticut Agriculture Experiment Station.
Once the farms began to be abandoned in the early 1900s, and as developers planted delicious shrubs around suburban houses, deer populations expanded. Now there are about 120,000 deer in Connecticut alone. They presumably cast a shower of black-legged ticks in their wake.
When the cause of Lyme disease was first worked out in the early 1980s, the solution to the problem seemed obvious: get rid of deer. As the deer population dropped, so would the incidence of Lyme.
But when wildlife managers put this solution into practice, it often didn’t work. That failure led scientists to a deeper understanding of the ecology that fuels the black-legged tick boom.
Black-legged ticks may prefer deer as adults, but as larva and nymphs they end up on smaller animals—probably because they can’t climb as high as adult ticks can. All told, black-legged ticks have been plucked off of some 175 species. They feed on birds, which can airlift them to new territory. And small mammals, like white-footed mice, nurture the younger generation of ticks.
Some of them also sustain Borrelia. The only way for the bacteria to endure is for older ticks to infect Borrelia-free larvae. Since deer don’t pick up many larvae, their Borrelia doesn’t spread very far.
White-footed mice, on the other hand, can become covered in larvae and nymphs. Better yet, their tiny bodies can build up huge concentrations of Borrelia, which doesn’t seem to make them sick.
Other hosts actually drive down tick numbers. Disease ecologist Rick Ostfeld and his colleagues at the Cary Institute have found that opossums are disastrous for black-legged ticks. Their immune systems kill off the pathogens that carry Lyme far more effectively than other species’ do, and they carefully groom their skin and devour any ticks they come across. A single opossum may kill 5,000 ticks every week.
Some species may even be able to control tick numbers and infection prevalence not by killing the ticks but by killing their favorite hosts. That is the new argument that Taal Levi, a postdoctoral researcher at the Cary Institute, put forward in a 2012 paper in the Proceedings of the National Academy of Sciences. After the morning tick drag, I sat down with Levi at a picnic table outside the institute to hear about the history of foxes.
Foxes were originally very abundant in the eastern United States, where they feasted on small mammals like white-footed mice. But the past few decades have not been good to them. “Fox harvests in the Northeast have declined substantially,” says Levi.
A number of studies suggest that coyotes have been responsible for the decline. Originally, foxes coexisted with wolves in the eastern and midwestern United States. Once wolves were eradicated, coyotes expanded from the Midwest to take their place. Coyotes kill foxes or scare them out of range.
Levi and his colleagues built a mathematical model of how these changes can affect rates of Lyme disease. When foxes disappear, the model suggests, numbers of small mammals like white-footed mice boom, feeding a growing population of ticks and their pathogens. For evidence, Levi points to historical records from sites across the Midwest and eastern United States. In some places, Lyme disease rates have gone up even though the deer population has not. But the rates in those places match up nicely with a decline in fox numbers.
Meanwhile, Williams and his colleagues at Lord Creek Farm are testing another idea about what’s driving Lyme disease. It occurred to Williams and his colleague Jeff Ward back in 2007. One day, while they were clearing a stand of Japanese barberry, they noticed something strange. “We said, ‘Wow, we’re really getting hammered with ticks,’” Williams recalls.
Williams and Ward speculated that the Japanese barberry was creating a miniature environment that favored ticks. So they began collecting tick specimens from barberry-infested sites around Connecticut, as well as from barberry-free sites. They also got rid of some barberry stands.
The results were striking. When the scientists dragged the barberry sites, they found 140 infected ticks per acre. Where they killed the barberry, they found only 40 ticks. And when they dragged places that were free of barberry, they found only ten.
“Look in there,” Williams says to me as we walk back to the truck at Lord Creek Farm. He points to an explosion of barberry. “Look how dense it is. Underneath that nastiness it’s really humid. A tick can hang out there and wait for a host.”
Williams and his colleagues have put humidity sensors in Japanese barberry stands to see how comfortable it is for a tick. For 23 or even 24 hours a day, it’s humid enough for questing and mating.
It’s too early yet for Williams to say how important Japanese barberry has been to the spread of Lyme disease. But he thinks it could be remarkable. He and Ward once dug up a map showing the distribution of Japanese barberry.
“We overlaid the Lyme disease data map over it,” says Williams. “It’s amazing how well it lines up.”
LAST YEAR I got to experience Lyme for myself. Or at least I think I did.
I began to feel unaccountably odd, with twinging aches around my shoulders and armpits. My doctor thought I seemed fine, but he raised his eyebrows when I mentioned that I had just taken my family on a weekend trip to Shelter Island, off the eastern end of Long Island. We’d spent a lovely afternoon hiking in the beautiful, tick-ridden Mashomack Preserve. Later I discovered that Mashomack is famous in the history of ticks: it was inside a tick collected on the preserve that Willy Burgdorfer discovered Borrelia.
My doctor prescribed antibiotics and sent me for a Lyme disease test. It seemed odd to me that he’d do both at the same time, rather than waiting for the test results before putting me on the drugs. But I went ahead and started taking doxycycline.
Ten days later, I went to my follow-up appointment. I felt fine. My doctor sat on a chair, resting a laptop on his thigh, and looked at my results on the screen.
“Well, you tested positive on the first test,” he said. “On the second test, you tested negative. Which is typical.”
The clearest sign that people have Lyme is that bull’s-eye of inflammation that forms around the tick bite. But many people don’t develop a ring, and others get it and fail to notice before it fades. Less than a third of people who get diagnosed with Lyme disease ever recall getting bitten by a tick. Those of us who feel odd but have no clear sign of Lyme must rely on a pair of unreliable tests.
In the first test, antibodies to Borrelia proteins are mixed into blood. If the antibodies grab onto the proteins, it’s time for the second test. That involves subjecting them to an electric current. Borrelia proteins travel at a distinctive pace compared with our own.
It’s a lousy way to diagnose a disease. The first test frequently delivers false positives, because the antibodies are too eager to grab onto proteins other than those of Borrelia. The second test frequently delivers false negatives, because the proteins fail to turn up in the right spot. So I may—or may not—have gotten Lyme.
Unfortunately, my experience is fairly typical when it comes to tick-borne diseases. The diagnosis is clumsy, the treatment often crude. One obvious way to deal with Lyme disease would be to give people a vaccine. And several drugmakers started developing Lyme vaccines not long after the disease was recognized. SmithKline Beecham brought a vaccine to market in 1998.
The vaccine fared poorly. It couldn’t be given to children, who are particularly prone to ticks, and in adults it provided only about 80 percent protection. Stories about arthritis-like symptoms caused sales to plummet, and SmithKline Beecham abandoned production. We are now in the strange situation where you can get your dog vaccinated for Lyme but you can’t get vaccinated yourself.
Even if the diagnosis and treatment of tick-borne diseases was more effective, we wouldn’t be able to eradicate them entirely. We humans are just a sideshow for ticks and their pathogens. The real action is happening out in our backyards, in our nature preserves, in abandoned lots behind strip malls. It’s there that ticks are proliferating on the animals that thrive in our landscapes. Instead of human medicine, perhaps we should try ecological medicine.
A number of researchers are doing just that. They’re building contraptions that can be filled with food for deer, mice, and other tick hosts. As the animals wiggle into the devices to eat, they rub against tick-killing ointments. Other researchers have put out vaccine-laden mouse bait, which would cause the mice to kill bacteria before they can spread to new ticks. Perhaps eliminating barberry would cut down on the tick population and reduce the rate of infection. Some researchers still think that wiping out deer should be part of the solution. And others have found fungi that can kill ticks in laboratory tests.
Entomologist Kirby Stafford has overseen tests of a number of these methods in Connecticut. Some work better than others, but at this point he doesn’t expect a panacea. “We’re never going to rid Connecticut of Lyme disease,” he says. “That’s the reality.”
Stafford, Williams, and their colleagues now have a grant from the CDC to try a kitchen-sink approach. In some sites, they’ll rip out barberry, apply tick-killing medicine, and vaccinate mice all at once. In others, they’ll leave out one or more treatments to see if their success changes. “You can tease out which treatment is having an effect,” Williams told me.
After Williams, Short, and Floyd finish their work at Lord Creek Farm, they plan to drive half an hour to set new traps in a forest in North Branford. Before leaving, Floyd leans out of the truck, holding out her thumb.
“Look,” she says, wiping it on Williams’s palm.
I can barely make out a mobile dot. “It’s like a moving freckle,” says Floyd.
We’re looking at a black-legged tick nymph, possibly loaded with some of Lord Creek Farm’s Borrelia and who knows what else. It tips forward and swiftly clamps into Williams’s skin. He tries to get his massive fingers around it as Floyd points out another nymph creeping up his arm.
Williams starts to curse as he gets rid of the two ticks. He then begins a full-on self-inspection, hoisting a boot on the rear bumper of the truck, smacking his legs.
“Sometimes,” he says, “you still get the heebie-jeebies.”
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