The Tick That Hunts Down Its Hosts—Including Us
It was a perfect day for a blood meal. A salt breeze blew over the western shore of Martha’s Vineyard, riffling the meadow grass under a pale-blue sky. They’d been waiting by the footpath all afternoon, crouched in the shade of a windswept cedar. They didn’t do well in the sun. They’d spent the winter half asleep, in the moist, rotting leaves under a huckleberry bush, well away from other creatures. But they were hungry now, as they always were in the spring. They’d scuttled out into the open air that morning and were sitting side by side on a blade of switchgrass, their tiny teardrop bodies barely bending it down. Their back legs gripped its serrated edge while their front legs reached toward the path, waiting for a warm body to lumber by. They looked like children at a Macy’s Parade, leaning out to touch the Snoopy balloon.
“Look at them sitting there,” a voice said. The ground shook beneath them and a giant face suddenly loomed above, its bulbous eyes inches from their bodies. They could smell the carbon dioxide in the air. “Just a little hot breath and they stick out their legs to latch on,” Patrick Roden-Reynolds said. He blew on the ticks again, and watched their front limbs spread wide, trembling in the current. Then he reached down with a pair of tweezers and plucked them off the grass. He stuck them on a lint roller and pressed them deep into the spongy plastic, next to the others he’d collected that afternoon. They were arranged in neat rows by sex and species—dog tick, deer tick, lone-star tick—eighty-one in all. “Everyone comes here and is afraid of Jaws,” he said. “That is not what you should be scared about. It’s the little things.”
Roden-Reynolds is thirty-three and has been the island’s public-health biologist for four years. To a hungry tick, he must have been an appetizing sight: tall, stout, and soft-featured, with pale red hair and eyebrows. His cheeks and hands were flushed pink with blood beneath the skin. But he knew better than to expose his other body parts. He was covered from neck to boots in fabrics soaked with permethrin—a pesticide modelled on the toxic pyrethrin found in chrysanthemum flowers. Had one of these ticks crawled up the cuff of his pants, it would have been dead before it reached his belt.
When he first came to Martha’s Vineyard, in 2022, Roden-Reynolds kept hearing that the ticks were worse than ever. But people had been saying that for years. The island had gone from farm and pasture in the nineteenth century to nature preserves and residential property in the twentieth, its silvery shingled homes encircled by forests and deer. The more bucolic it became, the more parasites it bred. “Every one of those deer could carry five hundred to a thousand ticks in a season,” Roden-Reynolds said. His predecessor, Dick Johnson, reckons that he got Lyme disease four or five times between 1990 and 2001. “It was no big deal,” Johnson told me. “Usually, they didn’t even give you a blood test.” The disease, caused by bacteria in deer ticks, can produce everything from flu-like symptoms to chronic fatigue and arthritis, if left untreated. But a dose of doxycycline or amoxicillin can generally cure it. In the early two-thousands, another tick-borne illness, babesiosis, began to make the rounds. Unlike Lyme disease, it didn’t respond to antibiotics alone, and its symptoms were more severe: chills, high fever, nausea, and, in rare cases, hemolytic anemia, a blood disorder that can be life-threatening. Then anaplasmosis joined the fray, spreading fevers and chills of its own. “People were getting knocked on their asses,” Johnson said. “Sometimes they’d get the trifecta of Lyme, babesiosis, and anaplasmosis, and end up in the I.C.U. fighting for their lives.”
The ticks on Martha’s Vineyard can now cause nearly a dozen different diseases. Lyme and babesiosis are eleven times more common than in mainland Massachusetts, and anaplasmosis is five times more common. Deer ticks were long responsible for most of the infections—nearly nine hundred cases of Lyme and babesiosis alone between 2020 and 2024. But those aren’t the ticks that locals fear most. Roden-Reynolds pointed to a row of stocky little bugs, each with a white dot on its back. These were lone-star ticks, first confirmed to be on the island in 2011. Most ticks are content to sit and wait for a meal to wander past; lone stars have no patience for that. “We see them actually pursuing hosts, which is really disconcerting,” one entomologist told me. Roden-Reynolds has found lone stars on walking trails and benches, in toolsheds, parking lots, and the yards of hundreds of local homes that he has surveyed. He has heard of them scrambling down dunes and across burning sand to feed on sunbathers. “Oh, they’re relentless,” he said.
To an outsider, the scene may spark a certain Schadenfreude, like an army of tiny barbarians sacking Rome. But the Vineyard is more than a wealthy enclave in this case. It’s a microcosm—part of a pattern of infestations and pest-borne diseases that has been repeated around the world, as climates have changed and landscapes have transformed. Fifty years ago, lone-star ticks rarely crossed the Mason-Dixon Line. Now they’ve marched as far north as Maine and as far west as the Oklahoma panhandle. One of the afflictions they bring, called alpha-gal syndrome, is the most rapidly spreading tick-borne illness in the country. Nature, it seems, is coming back to bite us.
In the summer of 2003, in a suburb of Sydney, Australia, a surfer went to see an allergist named Sheryl van Nunen. He was nineteen years old, tall and tan, with sun-bleached hair—“The sort of fellow you’d see on a beach in Gallipoli,” van Nunen told me—but he felt less than sprightly. Not long before seeing her, he had rushed to an emergency room in the middle of the night, his breathing ragged, his blood pressure low, his body covered in hives. He was having an anaphylactic reaction but didn’t know it. Van Nunen had seen such symptoms before, in patients going back for six years. The first was an older gentleman who had eaten a steak at a beachside restaurant in Sydney. The surfer, whose name was Jake, was the eleventh.
Van Nunen had asked Jake to bring in some leftovers from his last meal before the reaction. Now she poked a surgical lancet into each food item in turn, then pricked the skin of his right arm—a standard test for allergies. After a moment, the spot where she’d pricked him with a trace of cooked meat began to swell. It was a tiny welt—less than two millimetres in diameter—and Jake was unimpressed. Maybe the meat had some spice on it or was processed with a chemical? Van Nunen went to a refrigerator in her office and pulled out a tray of raw meats that she’d bought from an organic butcher—bits of beef and lamb. When she pricked the surfer again, this time after poking the raw beef, his skin swelled up ten times as much as before. Something had made him allergic to red meat.
The beaches and bush north of Sydney are full of peculiar beasts, like Martha’s Vineyard reimagined by Hieronymus Bosch: wobbegongs and jelly blubbers, swamp wallabies and fairy penguins, weedy sea dragons and beach worms up to nine feet long. Smaller creatures, too, can take alarming forms. The Australian paralysis tick, for example, doesn’t content itself with simply sucking its victims’ blood; it injects them with a neurotoxin that can be strong enough to kill a child if their symptoms go untreated. (In New South Wales alone, tick paralysis caused twenty deaths between 1900 and 1945.) The paths through the bush are infested with these ticks, as are many back yards. Six of the patients that van Nunen had treated for the meat allergy remembered being bitten by a paralysis tick. But their symptoms had appeared weeks or even months after the bite, and they were triggered hours after eating meat. The neurotoxin didn’t work that way—and most allergies didn’t, either.
By 2007, van Nunen had seen more than seventy patients with the meat allergy, many of whom had gone into anaphylactic shock. “I just thought, If this is an epidemic, we need to get the word out,” she told me. That fall, she presented a summary of twenty-five cases at a conference in Fremantle, south of Perth. The reaction was muted. “People were actually stunned,” she recalled. “They probably thought that I’d slipped off my trolley wheels.” Years later, van Nunen told me, when a colleague introduced her as a speaker at a panel in Sydney, she mentioned the presentation in Fremantle and said, “We thought she had gone entirely mad.”
Meanwhile, ten thousand miles to the northeast, an allergist and immunologist at the University of Virginia, Thomas Platts-Mills, was confronting a strange pattern of his own. He was investigating a drug called cetuximab, which contains genetically engineered antibodies that target cancer cells and prevent them from growing. In clinical trials, cetuximab had a good safety record—only three per cent of patients reacted poorly to it. But when it went to market, in 2006, it had a disturbing effect on patients in some areas. In clinics in Boston and California, the drug was well tolerated. But in North Carolina and Tennessee, nearly a quarter of the patients had severe reactions to the drug. In Arkansas, a patient died as it was being administered.
When Platts-Mills and his team studied blood samples from the reactive patients, they found allergy antibodies to a sugar molecule called galactose-⍺-1,3-galactose—alpha-gal for short. Most mammals have alpha-gal in their bodies, but humans and other primates do not. That’s one reason our immune systems reject transplant organs from pigs. Cetuximab is produced from both mouse and human DNA, so it does have some alpha-gal in it. But a single dose shouldn’t have been enough to trigger a reaction. And why were Southerners so susceptible?
As it happened, a few patients had come to the university clinic recently with a strange complaint: they seemed to be allergic to red meat. “It sounded made up,” Scott Commins, an allergy researcher at the University of North Carolina, told me. Commins was a post-doctoral fellow in Platts-Mills’s lab at the time and had been assigned to study the patients. “You’ve been eating hot dogs and hamburgers all your life, and all of a sudden you’re allergic to meat?” Most food allergies flare up within minutes of consumption, but these symptoms came hours after a meal. And the same patients weren’t allergic to chicken, turkey, fish, or seafood. What was different about pork and beef? “We were all reading about alpha-gal,” Commins told me. “So we started to say, ‘Holy shit! What if it’s related to that?’ ”
Humans and their ancestors have been eating red meat for millions of years. It seemed implausible that some cancer patients and carnivores would suddenly become allergic to it. Perhaps their immune systems were sensitized to alpha-gal by a local fungus, parasite, or pollen. The team had a map of patients who’d had allergic reactions to cetuximab—they were scattered across the Southeast, from Virginia to southern Missouri. But no other allergen seemed to have the same distribution. Then, in the summer of 2007, a research assistant named Jake Hosen got a hit. He was poring over maps of parasite-borne diseases when he came upon one for Rocky Mountain spotted fever, a disease often carried by dog ticks. It didn’t quite align with the cetuximab map—the cases stretched all the way to Boston—but it was close. So Hosen looked up the range of a Southern tick, the lone star, common as dirt in Virginia. That map was a perfect match.
“We were thinking, Can ticks do this?” Commins recalled. “So, I started feverishly calling all the people in my study. Ninety-three per cent had a tick history.” The final proof was provided, inadvertently, by Platts-Mills. In August of 2007, he was hiking in the Blue Ridge Mountains when he felt an odd, fuzzy feeling on his ankle. When he pulled down his sock, he saw what looked like hundreds of tiny seeds. Then they began to move. The seeds were a cluster of lone-star-tick larvae—a tick bomb, as it’s called—some of them already feeding on his blood. Over the next few weeks, Platts-Mills kept a record of his rising allergy antibodies. “He came in with the ticks in a Tupperware container,” Hosen told me. “And he said, ‘Draw my blood! Draw my blood!’ ”
That November—the same month that Sheryl van Nunen presented her tick theory to an incredulous audience in Australia—Platts-Mills went to a meeting in London. One night, for dinner, he ate three lamb chops and had two glasses of wine. A few hours later, he woke up in his hotel room feeling itchy. Then he watched, with some satisfaction, as his body broke out in hives. “Thus,” he later wrote, “the syndrome was now formally confirmed.”
Alpha-gal syndrome was an epidemiological novelty at first—an oft-told tale of far-flung scientists, baffling symptoms, and bloodthirsty ticks. Then it began to spread. The syndrome has now infected people in more than thirty countries on six continents. It can be found in Germany’s Black Forest and on small farms in South Africa, in the rain forests of Peru and the mountains of western Japan. Some tick species produce alpha-gal naturally in their saliva, which they inject into their host when they bite. In North America, the syndrome is transmitted mostly by the lone-star tick, but it seems to find new vectors wherever it goes. In Brazil, it’s carried by the Cayenne tick, in South Korea by the Asian longhorned tick, in Sweden and Norway by the castor-bean tick, and in Zimbabwe and Botswana by the South African bont tick. But its most effective carrier remains the paralysis tick. In Queensland and northern New South Wales, where most of the ticks live, the number of people with the syndrome is growing by forty-five per cent a year.
But those are just the known cases. Only a fraction of people with antibodies to alpha-gal become allergic to it, and those who are often don’t realize it. Some react only to red meat. Some also react to milk, cheese, and other animal products that have alpha-gal. The symptoms are so delayed that people often blame them on food poisoning, irritable-bowel syndrome, gluten intolerance. In the U.S., according to the Centers for Disease Control and Prevention, as many as half a million people have alpha-gal syndrome, but other researchers suspect that the number is higher. For years, testing was spotty at best, and doctors often weren’t aware of the syndrome. In a study published in 2017, fewer than one in ten alpha-gal patients were correctly diagnosed. In 2024, a New Jersey man died after eating a burger at a barbecue—the syndrome’s first documented fatality—and at least three other deaths might be linked to alpha-gal. There are likely to be more.
Could a syndrome so stealthy have lurked among us all along? Commins and van Nunen don’t think so. The surge in alpha-gal patients was too sudden and too great. Van Nunen has worked on Sydney’s North Shore for forty years. “Anyone who had anaphylaxis was sent to me, and I’ve talked to long-term residents,” she told me. “I know that patients didn’t have it before. It is an epidemic.” What triggered it still isn’t clear. Does the alpha-gal in a tick’s saliva piggyback on some virus or antigen that sensitizes people to it? “We lack a unifying hypothesis,” Commins said.
One thing is certain: ticks make excellent disease vectors, purpose-built for the modern world. They’re resistant to pesticides, partial to rising temperatures, and happy to feed on anything that moves—mice, deer, birds, hunters, hikers, suburbanites, and second-home builders. As cities have sprawled into countryside, and people have pushed deeper into nature, we’ve turned ourselves into a vast smorgasbord for ticks. Messing with their habitat seems only to make them multiply.
In the nineteen-nineties, the Australian government launched a national campaign to eradicate red foxes. British settlers had imported them more than a century earlier for hunts, only to watch them exterminate native species like the numbat, the boodie, and Gilbert’s potoroo. The fox-eradication campaign was deemed a huge success, but it came with another unintended consequence. As the foxes died, the ticks that had fed on them found another primary host—the shrewlike native bandicoot, which Australians had worked hard to reëstablish. “They became a nursery for ticks,” van Nunen told me. “It’s like Whac-A-Mole, trying to do something with nature.” The foxes went down; the bandicoots and meat allergies popped up.
Substitute bandicoots with white-tailed deer, paralysis ticks with lone stars, and you get the story of alpha-gal in America. Like the bandicoot, white-tailed deer were once an endangered species here, hunted nearly to extinction before the First World War. Then hunting laws were passed, habitats restored, deer reintroduced to their old territories. “We were an agrarian society and then we reforested the eastern United States,” Holly Gaff, a tick researcher and mathematical ecologist at Old Dominion University, in Virginia, told me. “Forest brings wildlife, wildlife brings ticks, and ticks bring disease.” The U.S. now has some thirty-six million deer, wandering the landscape like a fleet of mobile blood banks. “They can make infinite ticks, basically,” Gaff said.
Even states already teeming with bugs have begun to feel under siege. “Every year, we bring in new pests, and we still have all the same ones we had before,” Nancy Hinkle, a veterinary entomologist at the University of Georgia, told me. “It’s a never-ending battle.” Some pests come into the country on livestock and tropical fruit; others hitch rides on shipping crates, wooden pallets, foreign travellers and their pets. In Georgia, chicken farmers are beleaguered by bedbugs, which have hopped from hotel rooms to poultry farms, and from there to workers’ homes. In Texas, ranchers are bracing for an onslaught of screwworms, the flesh-eating maggots of blowflies. Before they were driven south out of the U.S. in the fifties and sixties, screwworms killed millions of deer and cattle, burrowing under their skin and into the navels of newborn calves and fauns. Now they’ve worked their way back north through Mexico to the Texas border. In more than two dozen states, meanwhile, farmers are fending off Asian longhorned ticks. First spotted on an Icelandic sheep in New Jersey in 2017, they can carry a deadly cattle parasite, Theileria orientalis. “We didn’t need another tick in Georgia,” Hinkle said. “We had twenty-two species already. That was a gracious plenty of them.”
The rise of the lone star may be the breaking point in this pest-ridden history. Like Lyme disease, named for a posh town in rural Connecticut, alpha-gal syndrome can seem like a symptom of privilege—of pampered city folks stepping out of their element. Martha’s Vineyard and the Hamptons have some of the highest alpha-gal rates in the country, but even there the people most at risk from infection may be outdoor workers. And the syndrome now threatens farmers, ranchers, hunters, and foresters across the South and the Midwest. “I have been standing up for thirty years saying, ‘If you get ehrlichiosis you could die,’ ” Gaff told me. “But if you say, ‘You might not be able to eat hamburgers or steak ever again,’ you suddenly get a reaction.”
Phillip James Ellison grew up in the bootheel of Missouri, wedged between eastern Arkansas and western Tennessee. “We come from crops,” he told me. “Cotton, dent corn, milo, soybean—that’s what I played in, as a kid in the fields. Then I moved up here to beef territory.” Missouri, Arkansas, and Oklahoma are the epicenter of alpha-gal in the United States. A study of blood samples from military recruits, taken between 2001 and 2007, found that nearly half the recruits from south-central Missouri, where Ellison lives, had allergy antibodies for alpha-gal. It’s not the best cattle country—scrubby pastures crisscrossed by tangled woods and limestone bluffs—but it’s ideal for ticks. Ellison’s wife, Kristie Byrd, belongs to a family that has run cattle east of Springfield for more than a century. When Ellison arrived, twelve years ago, he was put to work bottle-feeding the calves and transitioning them to grain. Then his body couldn’t take it any longer.
“I can’t even get near their dander anymore, or their wet nose or saliva,” he told me. “Whenever I handle one of them, I have to soak my hands—they’re so red and swollen.” The symptoms began not long after he moved to the area. Ellison would wake up with his stomach knotted, his skin crawling with a rash. It itched so badly sometimes that he would scratch himself bloody. “The doctors would say it’s lactose intolerance,” he told me. “You would not believe how many rounds of prednisone I’ve taken. Then I go to the dermatologist and he says, ‘Well, it’s just your eczema acting up.’ ” It was ten years before he was given a diagnosis of alpha-gal. “Basically, if it gives live birth and breast-feeds, I can’t touch it and I can’t eat it,” he said.
We were sitting in his Dodge Ram pickup, looking out over a fenced-in pasture. It was a damp gray evening in March, and a few cows and calves were huddled out in the cold, waiting to be fed. Ellison, who is fifty-five, was slouched behind the wheel with the heater blowing on him. He had on a rumpled, fleece-lined flannel shirt and a Peterbilt hat tugged low over his eyes. “I sell truck parts now,” he said. “I’m not allergic to truck parts.” He pointed to a calf standing off by itself. He was not only allergic to their dander and saliva; they could also carry lone-star ticks that could make his condition worse. The saddest part was not being able to give the calves treats anymore, he said. They used to trail after him as if he were their mom. “I was named for the disciples in the Bible, and I still follow the Ten Commandments,” he said. “But in that ten-year period when I didn’t know what was wrong with me, depression took over. I had bad thoughts. I told my mom, If I didn’t have a daughter and granddaughter, I would have gone home by now.”
The alpha-gal stories I’ve heard often play like scenes from horror films. The victims are unsuspecting, the settings innocuous: a burger joint, a picnic, a quiet night at home. A pregnant woman wakes up to find her husband leaning over her in the dark. “Something’s wrong,” he says. “My face doesn’t feel right. Could you go with me to the bathroom and look at it?” When she turns on the light, the left side of his face is so badly swollen that he’s nearly unrecognizable. An eleven-year-old girl comes home with her hands covered in blisters. There’s something weird in the school’s new soap, she tells her mom.
The syndrome is cryptic, unpredictable. It can lie dormant in the blood for years—even elevated allergy antibody levels may never trigger a reaction—then erupt with sudden violence. Without tick bites, red meat, or dairy to incite it, the immune response will subside eventually. After three or four years, you might even be able to eat a cheeseburger again. But if you live or work in the countryside, the opposite is more likely to happen. Another tick will latch on, and your immune system will reignite. The more bites you get, the more allergic you’ll probably become. At first, it may take a whole steak to set you off, then just the smell of bacon will do it. “I can’t go to restaurants with open grills anymore,” Michelle Kleeman, who owns a small farm an hour and a half west of Ellison’s place, told me. “My throat would be swelling from the smoke.”
In rural communities, alpha-gal doesn’t attack just the body. It attacks a way of life. Farming, ranching, hunting, raising and eating animals: everything you’ve been taught to do is suddenly bad for you. Even the landscape has turned toxic. Forty years ago, when the AIDS epidemic was ravaging New York, some Southern Baptists described it as God’s judgment—a punishment for its victims’ life style. I never heard alpha-gal described that way, but there were other, equally sinister explanations.
“I’m sure you’ve heard all the conspiracy theories,” Rick Blubaugh, an emergency-room doctor in Branson, Missouri, told me one morning, at a local diner. “There is a whole counterculture out there.” Lyme disease began as a biological weapon, one theory suggested. The bacterium that causes it, Borrelia burgdorferi, was named for the entomologist Willy Burgdorfer. During the Cold War, Burgdorfer did research for the U.S. military, infecting ticks for potential use as a bioweapon. But the Lyme-disease theory was soon debunked: Borrelia burgdorferi has been around since at least 1894, tick researchers pointed out, when some mice with the bacteria were collected on Cape Cod. Alpha-gal was more of a private enterprise, another rumor contends. Bill Gates, the co-founder of Microsoft, has invested heavily in lab-grown meats, which have no alpha-gal. His foundation has also funded research to genetically modify ticks to protect cattle. What if that work triggered the epidemic? “Covid got out of the lab. Did this get out, too?” Blubaugh said.
That theory has also been roundly dismissed: the research funded by the Gates Foundation wasn’t on lone-star ticks, and it had no relation to alpha-gal. Yet Blubaugh can see why the syndrome’s sudden rise seems suspect. When he started working in Missouri, twenty years ago, he almost never saw alpha-gal cases. “It’s almost daily now,” he said. People used to mistake the syndrome for other allergies; now they do the opposite. They come in with a rash, a stomach ache, a racing pulse, and assume that they’re allergic to meat. “They’ve already given themselves two or three epi shots and they say they need more,” Blubaugh told me. “And I think, Let’s hold off. Epinephrine makes you jittery and anxious, and your heart rate goes up. Maybe it’s causing the problem.”
True anaphylaxis is hard to mistake. When it seizes the immune system, the body goes haywire in a few ways at once. The skin may blister and the eyes inflame, the stomach knot up and the bowels loosen. If the throat and the tongue swell up, people often make an odd sound when they breathe in—a whistling squeak, or screech, known as stridor. “That’s when I’ll give epinephrine,” Blubaugh said. He gets a case like that almost every week, he told me. But that, too, gives him pause. “People have been getting bitten by ticks for thousands of years. Why are we seeing this disease all of a sudden?”
Matthew Overcast, a state representative for southern Missouri, didn’t believe in alpha-gal when he first heard about it from his family doctor. “I wouldn’t have said it was a conspiracy theory,” he told me. “But when he threw it out there I was, like, ‘Wait, what?’ ” Overcast has since become one of the country’s strongest advocates for alpha-gal awareness. When his oldest daughter, Lyla, was in kindergarten seven years ago, she began to suffer from escalating waves of symptoms: nausea, rashes, cramps, migraines, and easily fractured bones. Before her doctors diagnosed her with alpha-gal, they thought she might have leukemia or an autoimmune disease. “As a parent, you’re both pissed off and relieved when it turns out to be just an allergy,” Overcast said. Around that time, Lyla’s sister Adalynn began to get hives and stomach aches; then her brother Jackson came home with a rash on his face. Both were later diagnosed with alpha-gal, along with Overcast’s aunt, his youngest brother, and his wife, Jessica.
Last year, Overcast filed a bill with the Missouri legislature requiring labs to report and track all positive tests for alpha-gal. (It was passed in May and awaits the governor’s signature.) The data on blood samples from military recruits are twenty years old, and without up-to-date numbers it’s hard to know where and how to combat the syndrome. Twelve other states now track alpha-gal, and the preliminary numbers are alarming. In Virginia alone, since September, more than fourteen thousand people have tested positive for alpha-gal antibodies, most of them, probably, after showing symptoms of the allergy. On a per-month basis, that’s more than ten times the cases of Lyme disease recorded between 2010 and 2020—and Virginia’s alpha-gal rates aren’t nearly as high as Missouri’s.
It’s not clear what happens next. “I don’t see alpha-gal in the same light as measles or tuberculosis,” Blubaugh told me. “The data may help get more funding, but what’s the end goal? Can we cure it? Can we control it?” How do you stop an epidemic that seems to be everywhere and nowhere at once? That upends lives yet often goes undiagnosed? That requires wrenching social changes in how people eat, socialize, and move through nature? As Overcast put it, “It’s the only allergen you can’t avoid.”
Red meat and dairy are just the beginning. Animal products are woven so tightly, so microscopically, into what we consume that we often don’t know they’re there: Doritos, ramen, marshmallows, and frosted cereals; French fries cooked in beef tallow; tofu prepared on a grill that just had meat on it—even the most innocuous products can contain beef, pork, or dairy. The amount may be infinitesimal—white sugar and bottled water are sometimes purified with charred animal bones, for instance—but some hypersensitive alpha-gal patients avoid the risk anyway. They scan food labels for “natural flavoring”—industry shorthand, in many cases, for beef and pork extracts—the way other people scan for artificial coloring.
“When Lyla was first diagnosed, I cried in the grocery store,” Jessica Overcast told me. “I didn’t know what to feed her.” It was a weekday night, and the family was having dinner around the kitchen table. The Overcasts live an hour southeast of Springfield, in a small white farmhouse on a county road lined by forests and fields. Jessica, who is thirty-two and works for an online educational company, had made roasted salmon. While she talked, her four youngest, ages five to eleven, bounced and lolled and hotdogged around the kitchen, peering at me curiously, then dashing away. Lyla was baking boxed brownies for dessert. She was in seventh grade now, tall and skinny, with glasses, braces, and a bright, impish, self-possessed spirit.
“We’re really blessed that they like their vegetables,” Jessica said, putting some mashed broccoli and carrots on the table. “Even supplements can be difficult to know if they’re safe.” Iron and Vitamin B12 are often derived from beef organs, Vitamin D3 from lanolin secreted by the sebaceous glands of sheep. Other supplements come in gelatin capsules, made from collagen derived from cow and pig bones and hides, or mixed with dairy binders such as lactose and sodium caseinate. We wash our bodies with animal products (soap can contain tallow), brush our teeth with them (toothpaste can contain glycerin obtained from animal fat), and moisten our skin with them (lotions can contain lanolin, collagen, and tallow). “I always tell my husband, we have done an excellent job,” a rancher in Missouri, whose son has alpha-gal, told me. “I am so proud of how the beef industry has infiltrated every single thing.”
If there is one thing that would improve the lives of people with alpha-gal, Scott Commins told me, it’s better labelling: “Just tell us what’s in this stuff!” Drugs are a particular risk. When they’re injected into a vein, the allergic reaction can come within minutes rather than hours, and it can be life-threatening. Heparin, a common blood thinner, is extracted from pig intestines. Insulin can come from pig pancreases, estrogen from the urine of pregnant mares. Vaccines can contain amino acids or enzymes from beef. Antivenins for snakebites are made from horse blood. “The medical community is going to have to have a reckoning,” Lea Hamner, an epidemiologist on Martha’s Vineyard, told me. “Rabies is a hundred per cent fatal. Do you avoid the vaccine or risk the allergic reaction?” Even drugs that were once safe may have since been reformulated with animal products, she said. “Having to do that level of research on everything—that is a terrifying place to be.”
The Overcasts are old hands at avoiding alpha-gal by now. “It’s really not something you want to screw around with,” Matthew Overcast told me, at his house that night. “It can go from a moderate reaction to anaphylaxis like that.” He snapped his fingers. “We’re an hour’s drive from the hospital. We only have two EpiPens per kid, and you have to administer them every fifteen minutes. So, we’re kind of in a bind.” Last year, to keep some red meat in their diet, they took up emu farming. Seven of the prehistoric-looking birds were stalking around a pen outside, glaring at visitors as if we were the ones on the wrong continent. Inside the house, a plastic bin in the TV room held a striped emu chick, waddling under a heat lamp.
“We tried ostrich, but they died off in the first week,” Matthew said. Then, last spring, a tornado hit a local emu farm, and one of the birds got loose when his cage was destroyed. “He’d been wandering around for two or three months when we rescued him. We’re hoping to find an affordable way to produce them, but it’s a little bit of a challenge.” Their house sits on only an acre of land—when Overcast quit his job at a law firm to be a state representative, he took a six-figure pay cut—and the closest U.S.D.A.-certified slaughterhouse that will process the birds is in Arkansas. Still, for now, the meat is worth it. Emu is darker than beef and just as rich, yet it has no alpha-gal. “We did a blind taste test and a lot of people failed,” Jessica said.
“It tasted just like the real thing!” Lyla said. I asked her if she missed red meat. “Oh, definitely. Burgers! They just poofed out of existence, and I was, like, ‘Come back!’ ”
Red meat may one day be widely available for people with alpha-gal, but it probably won’t come from giant birds. Six years ago, the F.D.A. approved the first bioengineered, alpha-gal-free pig for human consumption. Bred by a biotech company called Revivicor, now owned by United Therapeutics, it was originally designed to provide organs for transplant. To prevent the organs from being rejected by their new human hosts, Revivicor deactivated a gene that codes for the enzyme that creates the alpha-gal molecule. A kidney from one of those pigs was the first to be transplanted into a human body, at N.Y.U. Langone Health, in 2021.
Eating the pigs was an afterthought. “We are very, very focussed on xenotransplantation,” John Bianchi, the vice-president for regulatory affairs at United Therapeutics, told me. The GalSafe pigs, as they’re called, are raised in an unmarked facility in rural Virginia, surrounded by razor wire and surveillance cameras. “We don’t want to invite any troublesome actors,” Bianchi said, when I went there in April. “There is incredible public concern and anxiety about gene-edited animals. But I think the GalSafe pig turns that upside down. Now all of a sudden you have a product that primarily benefits the consumer rather than the producer.”
My visit to the pig facility felt like touring a biohazard site. Codes were entered, security officers alerted, the car hosed off. To protect the pigs from contaminants and human pathogens, I had to change into sterile scrubs, rubber boots, and gloves, then dip my soles in a pan of disinfectant. Still, when I stepped inside the nursery, I found a drove of perfectly ordinary-looking pink pigs. They were four months old, trotting around in large pens with feed piped into bins from above. Some big rubber balls had been tossed in to keep them distracted. The gene editing had no effect on their health, Bianchi assured me, and they tasted just like other pigs. So far, only one company has been licensed to sell GalSafe pork: Amaroo Hills, based in North Carolina and Tennessee, which also raises emu. But word has spread in the meat-starved alpha-gal community. “I’m hoping to get my hands on a hog or two who have that gene removed,” Matthew Overcast told me.
The day before I visited the pigs, I’d tasted some GalSafe pork at the University of North Carolina. It was being served to an alpha-gal patient as part of a double-blind clinical trial organized by Scott Commins and Sarah McGill, a gastroenterologist at the medical school. McGill had chosen thirty patients who tested positive for alpha-gal and had symptoms of the syndrome. In previous weeks, they had twice come to the university and eaten a bowl of cooked ground pork. Then they waited six hours to see what happened. The pork looked identical on both visits, but one serving came from a regular pig, the other from a GalSafe pig. Neither the patients nor the researchers knew which was which.
The GalSafe pork I tasted was as ordinary as advertised, just a little bland for lack of spices. McGill and Commins expected it to have no allergic effect on their patients, and for the opposite to be true of the regular pork. But when McGill sent me her summary of the study later, the results were equivocal. The regular and the GalSafe pork caused allergic reactions at about the same rate—roughly twenty per cent of the time. The GalSafe caused only nausea and, in one case, faint flushing; the regular pork gave some patients hives, as well, and sent one woman to the hospital with recurrent vomiting. But most patients had no reaction to either meat.
“I have more questions than answers right now,” McGill told me. Were some of the patients false positives for alpha-gal? Did they have to eat meat more than once to reignite the allergy? Did their fear of a reaction alone make them react to the GalSafe pork? “It’s curious. It’s discordant,” she said. “I know that people can get way sick from alpha-gal, and I think it’s still underdiagnosed. But we’ve got a long way to go. It’s really humbling.”
Food intolerances are part mind and part body. They’re bound up in our habits and aversions, fears and imaginings. If you’re allergic to bees, a sting can kill you. But most allergies aren’t that extreme—they’ll give you hives but won’t stop your heart—and most intolerances aren’t allergies at all. You may get indigestion from gluten or lactose intolerance, but you’ll never go into anaphylactic shock. True allergies build up antibodies in the blood, which react to the presence of certain molecules. But even a system crawling with allergy antibodies sometimes needs another nudge before it attacks.
“I get tick bites, and I make low-level antibodies for alpha-gal,” Jeffrey Wilson, an allergist and immunologist at the University of Virginia, told me. “But I love to smoke brisket, and I never stopped. Why can I do that, and others end up in the emergency room?” Wilson believes that some reactions could be triggered by sources other than alpha-gal. He likens it to chronic urticaria, another condition that some of his patients have. “They break into hives for no rhyme or reason,” he said. A tick bite boosts allergy antibodies of all sorts, not just for alpha-gal. In some people, this could prime their system for reactions at any time, he said. “It’s like you have too much information in your body, and, with stress or other life things, you break out.”
Americans didn’t used to be this sensitive. Between 1997 and 2011, the rate of food allergies in children increased by fifty per cent, then did so again between 2007 and 2021. When I was in Missouri, I had lunch at a café in Springfield called the Safe Spoon. The menu was free of alpha-gal and of the nine most common food allergens—dairy, eggs, fish, peanuts, sesame, shellfish, soy, tree nuts, and wheat. “The term ‘vegan’ is basically a curse word around here,” the owner told me. Yet the place was packed. Many of the customers had more than one allergy, she said, and some hadn’t been able to share the same meal with their families for years.
Allergists themselves are partly to blame. For decades, they told new parents to keep peanuts and other allergenic foods out of their children’s diets. But the gut, it turns out, is extremely good at habituating itself to allergens. The skin and lungs are not. When children stopped eating peanuts, the allergens still found ways into their bodies. Between 1997 and 2010, peanut allergies quadrupled in the U.S.
Such overcaution is at the heart of three of the most popular explanations for the allergy epidemic: the hygiene hypothesis (we’ve stunted our immune systems by being too clean), the old-friends hypothesis (we’ve ravaged our gut biome with bad food and antibiotics), and the epithelial-barrier hypothesis (we’ve weakened the protective linings of our skin and lungs with disinfectants and other chemicals). But none of them can fully account for the rise of alpha-gal syndrome. “That is one of the fascinating things about it,” Commins told me. “It breaks all the allergy rules.” Some of the worst cases of the syndrome, for instance, have been on poor farmsteads in South Africa’s Eastern Cape. “They represent everything we’ve been told about nonallergic environments,” Commins said. “Dirt floors, babies without shoes, animals in the home, yet still you can become allergic.”
The results of the GalSafe-pork trial were, in some ways, par for the course. If you go into any classroom and draw blood from a hundred third graders, Commins said, fifteen or so will test positive for peanut antibodies, but only three or four will have symptoms when they eat peanuts. “This is a problem with all allergies,” he said. “I think it’s worse with alpha-gal because of the dang ticks.” Sometimes the antibodies can be stirred to action by exercise, alcohol, or a combination of the two. (In one German alpha-gal study, the researchers had some subjects drink a glass of wine or half a litre of beer and spin on a stationary bike.) Sometimes the antibodies just can’t be bothered.
Commins is working on a more definitive test for alpha-gal syndrome. In his lab at the university, he showed me a picture of a group of mast cells—the immune system’s first responders—as seen through a microscope. He called them Cluster 43. The cells had appeared in blood samples from patients with the syndrome after he activated their antibodies with an alpha-gal antigen. If the method could be automated, it could cut down drastically on false positives, Commins said. “It’s fancy but not otherworldly; the technology to do it could be there in three to five years.” It could also lead to more targeted treatments.
When Commins has patients who are highly allergic, he often prescribes Xolair. Originally approved for asthma, Xolair can also prevent severe reactions to food allergies. Some patients even eat meat while they’re on it, though it’s not yet approved for that use. Others swear by acupuncture that focusses on the nerves of the outer ear. “I’m fascinated by it,” Commins told me. “The best I can think of is that the needles are manipulating the signal from the vagus nerve—this master controller that has a branch that goes to the back of the ear. Mast cells sit at the end of nerve endings. So it may be that acupuncture somehow manipulates what the mast cell is sensing.” Allergists have always downplayed the role of the nervous system, he said. “But I think about my own kid. He eats a walnut and has hives within seconds. That has got to be the nervous system. Nothing else moves that fast. In my mind, that is where we are going. That is the next great thing.”
In the meantime, alpha-gal is a rare challenge to public health. It has no cure, no ironclad diagnosis or epidemiological data, and an expanding horde of ticks to spread it. The only way to stop them, Patrick Roden-Reynolds told me, when we were collecting lone stars on Martha’s Vineyard, may be to kill their hosts—to treat deer less like outdoor ornaments and more like supper. “You want my bold opinion?” he said. “We need to eat our way out of this problem.”
On my last day on the Vineyard, the leaders of the anti-tick campaign gathered on Zoom for a war council. Roden-Reynolds, the epidemiologist Lea Hamner, and Virginia Barbatti, the executive director of a nonprofit called Tick Free Martha’s Vineyard, were hunched over their laptops at locations around the island, scrutinizing a map of enemy encampments. Earlier that day, Barbatti’s group had released a sobering new survey of the island’s deer population. Using drones with heat-seeking sensors, it had located nearly five thousand deer on the island’s eighty-eight square miles of land—four times the deer density of central and western Massachusetts.
“Tick experts, when I tell them our deer density, they just laugh,” Hamner said. “They say, You don’t have a chance.” Hamner, who is thirty-three, is accustomed to places in crisis. Her father worked for U.S.A.I.D. in the Philippines; her mother worked for the World Health Organization there, and later did her doctoral research on sex workers in Peru. Hamner’s first jobs, after getting her master’s in public health at Yale, were in Washington State, where she was plunged into work on tuberculosis, opioid addiction, and then the pandemic. Skagit County, where she was based, had some of the first documented cases of COVID in the U.S., including fifty-two members of the Skagit Valley Chorale. In 2021, when Hamner moved to Martha’s Vineyard, where her husband was born and where she’d spent summers as a girl with her grandparents, she wasn’t expecting to work on public health right away. “I really needed a break,” she told me. Then came alpha-gal.
“This is an existential threat,” Hamner said. “Not just to our health and well-being, but to our economy. People will leave and not come back.” The taxes paid by second-home owners keep the island’s public services afloat, and most businesses survive on tourism in the summer months—when all the ticks come out to feed. “People with alpha-gal will be the ones to leave first,” Hamner said. “To have a chance to get over their allergy, they need to not get more tick bites.” Barbatti nodded. “There is this sense of, Am I putting my kids at undue risk?” she said. “Are we going to have a generation of kids going to college with EpiPens?”
Martha’s Vineyard is more than a microcosm of the epidemic. It’s a testing ground for addressing it, Hamner said. “An island is a controlled environment to do experiments and then scale out. We have high need, high burden, high impact, and we really need to incubate a solution. Once we get the blueprint, we can go to, How do you translate this to Missouri?”
The first impulse, for many locals, is to smother their yards in pesticides. But that almost never works. Lone stars can tolerate many poisons, and, even when they can’t, there are always more ticks next door to replace them. “You can’t spray a whole city,” Holly Gaff, the tick researcher at Old Dominion, told me. Gaff and a team of engineers at Virginia Military Institute have designed a TickBot—a sort of outdoor Roomba—that can drag a permethrin-soaked cloth around a lawn. Another device, called a 4-Poster bait station, attacks the ticks that congregate on deer’s heads. When deer bend down to eat the bait, paint rollers cover their heads in permethrin. But those are stopgaps at best.
“Zoom in on the deer locations,” Roden-Reynolds said. He blew up the shared map on his screen and moved his pointer to a dark, amorphous area fringed with bright-yellow dots. “Compare the conservation areas to the neighborhoods,” he said. “Look at Peaked Hill Reservation. It has a few deer, but the neighborhoods around it are just loaded.” Red Gate Farm, Jackie Onassis’s old estate, was especially popular. Deer aren’t idiots, Roden-Reynolds said. Hunting is allowed in conservation areas, but illegal within five hundred feet of an occupied house without the owners’ permission, so the deer go where they won’t be shot. He zoomed the map out again. All over the island, the residential areas were clustered with dots, along forest edges and around people’s yards. By day, the deer stay close to the houses, but not too close. At night, they move in and eat the hydrangeas.
Truly controlling the ticks will take an island-wide killing spree, the war council agreed. Deer numbers will have to drop by at least seventy per cent—more than three thousand animals. Local hunters, by all accounts, are ready and able. The hunting season has been lengthened by nearly two months, and there is no bag limit on does. Tick Free Martha’s Vineyard plans to build a processing facility for the carcasses; the meat, most of it donated to a local food pantry, is in high demand. “This island elevates fishermen. It elevates farmers,” Barbatti said. “This is our opportunity to elevate the hunting community.”
The deer are easy pickings for now. Roden-Reynolds is a bow hunter. In the sixteen years before he moved to the island, he shot a total of four deer. Now he shoots five a year. Hamner’s in-laws have a family hunting camp that killed fifty in one week this past fall. “They think they did bad if they shoot forty,” she said. But the fewer deer there are, the harder the hunting will be. In the late nineties, when Lyme disease swept over Monhegan Island, off the coast of Maine, a professional sharpshooter was brought in to kill every single deer. The campaign worked: the tick population plummeted. But Martha’s Vineyard won’t go that far—not yet, anyway. “This is just step one,” Barbatti said. “It is the lever that is available to us now.”
In the meantime, like the paralysis ticks in Australia, the lone stars will find other hosts to feed on, such as short-tailed shrews and white-footed mice. “There are plenty of little nurseries out there,” Nancy Hinkle, the veterinary entomologist in Georgia, told me. “Possum, raccoons, dogs, cats, rodents, foxes, skunks, us.” Nothing can match deer for hosting ticks, so the lone-star population will drop, but it will never go away. “They’ll survive long after we do,” Hinkle said. “They’ll survive after nuclear annihilation.”
Late that night, I walked back to my hotel in Vineyard Haven, relieved to be heading home the next morning. I’d spent the past few months in some of the country’s most beautiful landscapes—the Ozarks, the Blue Ridge Mountains, and this bright, windblown island—but always with a vague sense of unease. Every passing lawn and meadow, every winding path through the woods, seemed to hide a lurking menace. That may be what’s hardest to bear about alpha-gal: how it puts us at odds with nature, makes us distrust our most beloved places. It would be good to be back in New York City, I thought, in the relative safety of brick and concrete.
Wishful thinking, as it turned out. A health alert from the city later informed me that lone-star ticks are now comfortably settled on Staten Island and parts of the Bronx. Eastern Long Island has been overrun for decades, and Brooklyn could be next. All it would take is a tick bomb or two to infest Prospect Park, three blocks from my house. The barbarians are crawling toward the gate. ♦