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One type of tick can make people allergic to red meat — and it seems to be spreading

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One type of tick can make people allergic to red meat — and it seems to be spreading




There are a lot of disturbing things about the allergy to red meat and other mammal products spread by bites from the Lone Star tick.


There's the allergy itself, which has often been described as a red meat allergy, but really can be an allergy to mammal products — including dairy products or potentially even animal byproducts that appear in gel-cap pills and medications with antibodies derived from animals. There's the new discovery that the allergy seems to be linked to a higher risk of heart disease, according to a recent study.


There's the fact that the allergy can be severe enough to trigger an anaphylactic reaction, which can be life threatening and requires the use of an Epi-Pen.


And there's the timing of the allergic reaction. With most food allergies, it takes only 15 or 20 minutes after exposure for severe reactions to occur. Not with this one.


"The weird thing about [this reaction] is it can occur within three to 10 or 12 hours, so patients have no idea what prompted their allergic reactions," Dr. Ronald Saff, an allergist in Tallahassee, Florida, and an assistant clinical professor at the Florida State University College of Medicine, told Business Insider.


"They're sleeping, and they have no idea what they could be allergic to because the symptoms occurred so many hours after going to bed," Saff said.


But perhaps most disturbing is that we don't know how common this allergy is, but we have good reason to think it's spreading.


The alpha-galactose (or alpha-gal) allergy is still new enough that it's not counted by the CDC on its lists of tick-borne diseases. But we do know that tick-carried disease rates are skyrocketing in the US, as a recent Centers for Disease Control and Prevention (CDC) reportrevealed.


Ticks are spreading to new areas, enabled in some cases by warmer weather that expands their habitats and extends tick season longer into the fall, according to CDC officials. Tick diseases are also are spreading rapidly, according to that recent report, because ticks are much harder to control and kill than other blood-sucking pests.


The same things are true about the ticks that spread these allergies.

Lone Star Tick RangeIt's possible the Lone Star tick has expanded beyond these regions, this CDC map was last revised in 2011.  CDC

"Quite aggressive" biters

The Lone Star tick that spreads this allergy is named for the shape of the white splotch on the back of adult females. Lone Star ticks at all stages of life bite humans — even the tick's larvae, unlike with all other American ticks — and can be "quite aggressive," according to the CDC. The tick also feeds on and may catch a ride on cats and dogs.


The Lone Star tick is most common in the Southeast, but in recent years it has spread up the East Coast and into the Midwest, with large numbers reported all the way up in Maine. Within the last two years, outbreaks of alpha-gal allergy have occurred in Minnesota, New Hampshire, and on the tip of Long Island.


Much about the Lone Star tick and alpha-gal is a mystery. We know something in the tick's bite causes changes in people that make them sensitive to a sugar compound (alpha-galactose) that exists in mammal products. Certain people develop more sensitivity than others, and a few can tolerate small amounts of meat, but some become so allergic that they can't even consume animal products like dairy milk.


No one knows for sure whether the allergy goes away with time, but scientists think that both additional tick bites and meat consumption might worsen the condition.


The distribution, range, and abundance of Lone Star ticks have all increased over the past 20 to 30 years, according to the CDC. And warmer summers could make that situation even worse.


We expect with warming temperatures, the tick is going to slowly make its way northward and westward and cause more problems than they're already causing," Saff said.

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For years, nothing about Tami McGraw’s life has been normal. She cannot eat beef or pork, or drink milk or eat cheese or snack on a gelatine-containing dessert without feeling her throat close and her blood pressure drop. Wearing a wool sweater raises hives on her skin; inhaling the fumes of bacon sizzling on a stove will knock her to the ground.


Everywhere she goes, she carries an array of tablets that can beat back an allergy attack, and an auto-injecting EpiPen that can jolt her system out of anaphylactic shock.

McGraw is allergic to the meat of mammals and everything else that comes from them: dairy products, wool and fibre, gelatine from their hooves, char from their bones.


This syndrome affects some thousands of people in the USA and an uncertain but likely larger number worldwide, and after a decade of research, scientists have begun to understand what causes it. It is created by the bite of a tick, picked up on a hike or brushed against in a garden, or hitchhiking on the fur of a pet that was roaming outside.


The illness, which generally goes by the name ‘alpha-gal allergy’ after the component of meat that triggers it, is a trial that McGraw and her family are still learning to cope with. In much the same way, medicine is grappling with it too.


Allergies occur when our immune systems perceive something that ought to be familiar as foreign. For scientists, alpha-gal is forcing a remapping of basic tenets of immunology: how allergies occur, how they are triggered, whom they put in danger and when.


For those affected, alpha-gal is transforming the landscapes they live in, turning the reliable comforts of home ­– the plants in their gardens, the food on their plates – into an uncertain terrain of risk.


One time, Tami McGraw took capsules of liquid painkiller and woke up in the middle of the night, itching and covered in hives provoked by the drug’s gelatine covering.


When she bought an unfamiliar lip balm, the lanolin in it made her mouth peel and blister.


She planned to spend an afternoon gardening, spreading fertiliser and planting flowers, but passed out on the grass and had to be revived with an EpiPen. She had reacted to manure and bone meal that were enrichments in bagged compost she had bought.


She struggled with the attacks’ unpredictability, and even more with the impact on her family. “I think I’m getting better, and then I realise I’m not,” she says. “I’m more knowledgeable about what I can and can’t do.”


The story begins with a cancer drug called cetuximab, which came onto the market in 2004. Cetuximab is a protein grown in cells taken from mice. For any new drug, there are likely to be a few people that react badly to it, and that was true for cetuximab. In its earliest trials, one or two of every 100 cancer patients who got it infused into their veins had a hypersensitivity reaction: their blood pressure dropped and they had difficulty breathing.


That 1–2 per cent stayed consistent as cetuximab was given to larger and larger groups. And then there was an aberration. In clinics in North Carolina and Tennessee, 25 of 88 recipients were hypersensitive to the drug, with some so sick they needed emergency shots of epinephrine and hospitalisation. At about the same time, a patient who was receiving a first dose of cetuximab in a cancer clinic in Bentonville, Arkansas, collapsed and died.


The manufacturers, ImClone and Bristol-Myers Squibb, checked every obvious thing about the trial: the drug’s ingredients, the cleanliness of the manufacturing plants, even the practices at the medical centres where cetuximab had been administered. Nothing stood out. The most that researchers could guess at the time was that the unlucky recipients might have some kind of mouse allergy.


Then the first coincidence occurred: a nurse whose husband worked at the Bentonville clinic mentioned the death to Dr Tina Hatley, an immunologist in private practice in Bentonville. Hatley had recently finished postgraduate training at the University of Virginia’s allergy centre, and she mentioned the death to her former supervisor, Dr Thomas Platts-Mills.


The bad responses to the drug looked like allergic reactions, and they were common enough – and far enough from the manufacturer’s expectations – to be an intriguing research opportunity.


Platts-Mills pulled together a team, looping in Hatley and several current research fellows as well. Fairly quickly, they discovered the source of the problem. People were reacting to the drug because they had a pre-existing sensitivity, indicated by a high level of antibodies (called immunoglobulin E, or IgE for short) to a sugar that is present in the muscles of most mammals, though not in humans or other primates. The name of the sugar was galactose-alpha-1,3-galactose, known for short as alpha-gal.


Alpha-gal is familiar to many scientists because it is responsible for an enduring disappointment: its ability to trigger intense immune reactions is the reason that organs taken from animals have never successfully been transplanted into people. The puzzle was why the drug recipients were reacting to it. To have an allergic reaction, someone needs to have been primed with a prior exposure to a substance – but the trial recipients who reacted badly were all on their first dose of cetuximab.


Team members scrutinised the patients and their families for anything that could explain the problem. The reactions appeared regional – patients in Arkansas and North Carolina and Tennessee experienced the hypersensitivity, but ones in Boston and northern California did not. They investigated parasites, moulds and diseases that occur only in pockets of the USA.


Then Dr Christine Chung, a Nashville researcher recruited to the team, stumbled on an intriguing clue. Almost one in five of the patients enrolled at a cancer clinic at her hospital had high levels of IgE to alpha-gal. But when she checked those patients’ near neighbours, treating them as a control group – that is, people who lived their lives in the same way, but did not have cancer and had no reason to have received the drug – almost one in five had antibodies to alpha-gal as well.

Almost a decade later, that correlation still makes Platts-Mills chuckle. The alpha-gal reaction “had nothing to do with cancer,” he says. “It had everything to do with rural Tennessee.”


The question then became: what in rural Tennessee could trigger a reaction like this? The answer arose from a second coincidence. Dr Jacob Hosen, a researcher in Platts-Mills’s lab, stumbled across a map drawn by the Centers for Disease Control and Prevention (CDC) showing the prevalence of an infection called Rocky Mountain spotted fever. It exactly overlapped the hot spots where the cetuximab reactions had occurred.


Rocky Mountain spotted fever is transmitted by the bite of ticks, including Amblyomma americanum, one of the most common ticks in south-eastern USA. It’s known as the lone star tick for a blotch of white on the back of the female’s body.


The researchers wondered – if the mystery reactions shared a footprint with a disease, and ticks caused the disease, could ticks be linked to the reactions too?

It was an intriguing hypothesis, and was reinforced by a new set of patients who came trickling into Platts-Mills’s clinic at about the same time. They were all adults, and that was odd to start with, because allergies tend to show up in childhood. They had never had an allergic reaction before, but now they were experiencing allergy symptoms: swelling, hives and in the worst cases anaphylactic shock. They too had high levels of IgE antibodies to alpha-gal.


None of them, though, were cancer patients. They told the physicians that they had no proof of what was causing their reactions – but more than a few of them sensed it had something to do with eating meat.


Dr Scott Commins, another postgraduate fellow in Platts-Mills’s group, took it upon himself to phone every new patient to ask whether they’d ever suffered a tick bite. “I think 94.6 per cent of them answered affirmatively,” he says. “And the other few per cent would say, ‘You know, I’m outdoors all the time. I can’t remember an actual tick that was attached, but I know I’d get bites.’”


Meat from mammals inevitably contains alpha-gal – so in already sensitised individuals, eating meat might constitute a second exposure, in the same way infusing cetuximab had been.


If tick bites had sensitised them, then the alpha-gal reaction might be a food allergy as well as a drug reaction. But the connection was speculative, and cementing cause and effect would take one final, extraordinary coincidence.


As it happens, Platts-Mills likes to hike. One weekend he took off across the central Virginia hills, tramping through grassy underbrush. He came home five hours later, peeled off his boots and socks, and discovered his legs and feet were speckled with tiny dots. They looked like ground pepper, but they were dug into his skin – he had to use a dull knife to scrape them off – and they itched something fierce. He saved a few, and sent them to an entomologist. They were the larval form of lone star ticks.


This, he realised, was an opportunity. As soon as the work week started, he had his lab team draw his blood and check his IgE levels. They were low to start with, and then week by week began to climb. Platts-Mills is English – his father was a Member of Parliament – and in the midst of having his IgE tracked, he went to an event at the Royal Society of Medicine in London.


“And at that point,” he says cheerfully, “I ate two lamb chops and drank two glasses of wine.”


In the middle of the night, he woke up covered in hives.


There has been so little research into alpha-gal allergy that scientists can’t agree on exactly what stage of the bite starts victims’ sensitisation. It is possible that a fragment of a previous blood meal, from a mouse, bird or deer, lingers in a tick’s guts and works its way up through its mouth and into its human victim. It’s also possible that some still-unidentified compound in tick saliva is chemically close enough to alpha-gal to produce the same effect.


One aspect of its epidemiology is becoming clear, though. The allergy isn’t only caused by the lone star tick. 


In Australia, Van Nunen (who is now a clinical associate professor at the University of Sydney School of Medicine) couldn’t understand how her patients’ tick bites solved the mystery of their meat allergy. But she could see something else. The beaches that fringe the coast north and south of Sydney are rife with ticks. If bites from them were putting people at risk of a profound allergy, she felt compelled to get the word out.


In 2007, Van Nunen wrote up a description of 25 meat-allergic patients whose reactions she had confirmed with a skin-prick test. All but two had had severe skin reactions to a tick bite; more than half had suffered severe anaphylaxis. That abstract formed the basis of a talk she gave later that year to an Australian medical association, which was then indexed – but not published in full – in an Australian medical journal. It took until 2009 for the Virginia group to catch up to it, after they had already published their first alert.


And so it has proved. Alpha-gal reactions linked to tick bites have now been found in the UK, France, Spain, Germany, Italy, Switzerland, Japan, South Korea, Sweden, Norway, Panama, Brazil, Côte d’Ivoire and South Africa. These cases trace back to at least six additional tick species. (An online map on which patients list themselves includes over a dozen more countries.)


Wherever ticks bite people – everywhere other than the Arctic and Antarctic – alpha-gal allergy has been recorded. In Belgium, patients reacted badly to a drug produced in rabbit cells. In the Italian Alps, men who went hunting in the forests were more at risk than women who stayed in their village. In Germany, the most reactive food was a traditional delicacy, pork kidneys. In Sweden, it was moose.


Van Nunen herself has now seen more than 1,200 patients. “The next busiest clinic, about 350,” she says. Those cases have all occurred in two decades, less than the span of a single human generation. As in America, the surge leaves Van Nunen mystified as to what the cause might be. She reasons that the rise cannot be due to something in her patients; neither genetic nor epigenetic change could occur so quickly.


“It has to be environmental,” she says.

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