Allergic reaction sparks award-winning science fair project for Missouri teen
An increase in the Lone Star tick population since 2006, and the ability to recognize the ticks as the source of “alpha gal” allergy to red meat has meant significantly more cases of anaphylaxis being properly identified.
A new study in Annals of Allergy, Asthma and Immunology, the scientific publication of the American College of Allergy, Asthma and Immunology (ACAAI) showed that at the University of Tennessee Health Science Center, alpha-gal ( a complex sugar found in red meat from beef, pork, venison, etc.) was the most common known cause of anaphylaxis. In previous studies of anaphylaxis, researchers were often unable to identify the source of the severe allergic reaction.
“Of the 218 cases of anaphylaxis we reviewed, 33 percent were from alpha gal,” says Debendra Pattanaik, MD, lead author of the study. “When we did the same review in 1993, and again in 2006, we had a great many cases where the cause of the anaphylaxis couldn’t be identified. That number of unidentified cases dropped from 59 percent in 2006 to 35 percent in this report – probably from the number of identified alpha gal cases. Our research clearly identified alpha gal as the cause of anaphylaxis in the majority of cases where the cause was detected. Food allergies were the second leading cause, accounting for 24 percent.”
The people in the study were seen between 2006 and 2016. The study notes that alpha gal allergy was first identified in 2008, so previous reviews wouldn’t have taken it into consideration. Due to increased awareness of red meat allergy, and more diagnostic testing available, alpha gal allergy went from an unknown entity to the most commonly identified cause of anaphylaxis at this center.
“We understand that Tennessee is a state with a big population of Lone Star ticks, and that might have influenced the large number of alpha gal cases we identified,” says allergist Jay Lieberman, MD, vice chair of the ACAAI Food Allergy Committee and a study co-author. “The Lone Star tick is predominantly found in the southeastern United States and we would expect a higher frequency of anaphylaxis cases in this region would be due to alpha gal. However, the tick can be found in many states outside this region and there are already more cases being reported nationwide.”
The remainder of the cases of anaphylaxis in the study were attributed to insect venom (18 percent) exercise (6 percent) systemic mastocystosis (6 percent) medications (4 percent) and other (3 percent).
A bite from the Lone Star tick can cause people to develop an allergy to red meat, including beef, pork and venison. The allergy is best diagnosed with a blood test. Although allergic reactions to foods typically occur rapidly, within 60 minutes of eating the food, in the case of allergic reactions to alpha-gal, symptoms often take several hours to develop. Because of the significant delay between eating red meat and the appearance of an allergic reaction, it can be a challenge to connect the culprit foods to symptoms. Therefore, an expert evaluation from an allergist familiar with the condition is recommended.
Allergists are specially trained to test for, diagnose and treat allergies. To find an allergist near you who can help create a personal plan to deal with your allergies and asthma, use the ACAAI allergist locator.
For more on Alpha Gal: https://madisonarealymesupportgroup.com/2017/01/12/tick-related-red-meat-allergy-found-in-minnesota-wisconsin/ Yes, Martha, it’s here in Wisconsin.
https://madisonarealymesupportgroup.com/2018/05/04/arkansas-woman-develops-deadly-meat-allergy-after-tick-bite/ As Meritt points out on the Allergy & Asthma Clinic of Northwest Arkansas’ website, the alpha-gal allergy extends to beef, pork, gelatin and products that contain mammalian ingredients. “That includes dairy products,” Burton said. “Mammal biproducts are in everything — daily vitamin supplements, shampoo, conditioners, hand and body lotions … all those things were keeping my system agitated. Pork or beef would just put it over the edge.”
A lot of vaccines are either made with animal products or have gelatin in it.
Entomologist Larry Dapsis, Deer Tick Project Coordinator, of Cape Cod Cooperative Extension presents information about numerous types of ticks and the diseases they carry in the following Tickology video series.
For more on tick prevention: https://madisonarealymesupportgroup.com/2017/05/11/tick-prevention-and-removal-2017/
https://madisonarealymesupportgroup.com/2018/05/27/study-conforms-permethrin-causes-ticks-to-drop-off-clothing/ “All tested tick species and life stages experienced the ‘hot-foot’ effect after coming into contact with permethrin-treated clothing,” Eisen said.
https://madisonarealymesupportgroup.com/2018/04/03/fire-good-news-for-tick-reduction/ Study found a 78-98% reduction in ticks.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0112174 These data indicate that regular prescribed burning is an effective tool for reducing tick populations and ultimately may reduce risk of tick-borne disease.
His wife wasn’t home, so he drove himself to the university hospital emergency room near where he lived in Chapel Hill, N.C. As he explained his symptoms at the check-in counter, he began to feel faint, then fell to one knee. An orderly offered a wheelchair. He sat down — and promptly lost consciousness.
When he came to, he was on the floor. He had rolled out of the wheelchair and hit his head. A gaggle of worried-looking medical staff stood over him. They asked if he was on drugs. Did he have heart problems? His blood pressure was extremely low, probably the reason he had passed out. Niegelsky, who was 58, told them that he was healthy and drug-free and had no heart condition.
“I could see the concern on their faces in a way that did not help my confidence level at all,” Niegelsky says.
He felt as if insects were biting every inch of his hands, armpits and groin. A doctor asked if he had any food allergies. The hives and the low blood pressure suggested anaphylaxis, a severe allergic reaction. Again the answer was no, but Niegelsky did recall that he had a very bad allergic reaction a month earlier to a tick bite he got at a concert.
The E.R. doctor ordered two shots of epinephrine, a form of adrenaline that dampens the allergic reaction; the hives and itching began to subside about 25 minutes later. Now the doctor asked Niegelsky what he’d eaten that day. A hamburger for lunch, Niegelsky told him. In his recollection, the doctor’s eyes widened, and he said,
“I think we know what you have” — a condition called mammalian-meat allergy.
Meat allergy was first observed in the 1990s and formally described in 2009, which makes it a relatively recent arrival to the compendium of allergic conditions. Its most curious quality may be that it is seemingly triggered by a tick bite. In America, the culprit, called the lone-star tick — females have a distinctive white splotch on their backs — is common in the warm and humid Southeast, where most cases of meat allergy have been diagnosed. Niegelsky had in fact heard about the allergy from friends. He remembers shaking his head and thinking that it sounded “made up.” He understood now, in a visceral way, how real it was. That bite from a month ago had primed his body for today’s hives and plummeting blood pressure.
Mammalian-meat allergy “really has the potential to revolutionize our understanding of food allergy, because it doesn’t fall under the umbrella of our paradigm,” Dr. Maya R. Jerath, a professor of medicine at Washington University School of Medicine, in St. Louis, told me. “Maybe our paradigm is wrong.”
“Six hours later I was in a hotel, covered in hives, itching like crazy and laughing at myself,” he told me. By then, he thought he knew what was happening: The ticks had made him allergic to those chops.
“This is really allergy in a kit — how to get it and how to lose it,” van Nunen said. “There’s really nothing else like it.”
Mammalian-meat allergy differs from most other food allergies in several important ways. One is the delayed reaction; it’s not uncommon for sufferers to wake up in the middle of the night, hours after a steak dinner, covered with hives and struggling to breathe. By contrast, those with food allergies to peanuts usually develop symptoms within minutes after ingesting the offending food. And whereas in most cases of allergy, the immune system pursues a protein, meat allergy is set off by a sugar.
Another unusual aspect of meat allergy is that it can emerge after a lifetime spent eating meat without problems. In other food allergies, scientists think that children’s immune systems may never learn to tolerate the food in the first place. But in meat allergy, the tick seems to break an already established tolerance, causing the immune system to attack what it previously ignored. One way to understand how the parasite pulls this off is to consider its bite as a kind of inadvertent vaccine. A vaccine teaches an immune system to pursue a pathogen it otherwise wouldn’t by exposing it to weakened versions of that pathogen — an attenuated measles virus, say — or bits and pieces of dead pathogen. Vaccines also often contain a substance called an adjuvant, which is designed to spur the immune system into action.
In similar fashion, when the lone-star tick feeds, alpha-gal leaks from its mouth into the wound, exposing the victim’s immune system to the sugar, prompting the immune system to remember and pursue alpha-gal. But exposure to alpha-gal alone probably doesn’t achieve this feat. Commins, who is at the University of North Carolina, at Chapel Hill, has identified a candidate, an enzyme in the tick’s saliva called dipeptidyl-peptidase that works as an adjuvant. It’s also common in bee and wasp venom. This enzyme, Commins argues, is what tells your immune system to see alpha-gal as the type of threat that warrants the itching and swelling of the allergic response.
Once sensitized, some victims find that they can no longer tolerate beef, pork, lamb — even milk or butter, foodstuffs with only very small amounts of alpha-gal. Several factors can also affect the severity of the allergic reaction, or if there is an allergic reaction at all. Grilled meat is less allergenic than other methods of preparation that preserve more of its fat. Fatty meat leads to more alpha-gal crossing a person’s gut barrier into his or her circulatory system, triggering a stronger immune reaction than leaner cuts. A study of German patients also found that alcohol imbibed with meat can push people toward an allergic reaction, as can exercise; both actions make the gut more permeable, exposing the immune system to more alpha-gal.
As it happens, an immune response to alpha-gal is also what drives, in part, the rejection of tissue transplanted from animals to people.
A recent study by scientists at the National Institutes of Health, which included Commins and Platts-Mills as co-authors, linked allergic sensitization to alpha-gal with a greater risk of arterial plaques, a hallmark of heart disease. It’s unclear whether having alpha-gal antibodies specifically increases your risk of developing plaques or whether some other factor increases a person’s risk of heart disease and sensitization to alpha-gal. But if it turns out that meat allergy pushes people toward cardiac arrest, it would imply that encounters with the lone-star tick contribute to the leading cause of death in the United States.
The big, unanswered question is why meat allergy is on the rise today. Commins estimates that at least 5,000 cases have been diagnosed in the United States, and many more probably remain undiagnosed. In some tick-heavy regions, the prevalence of meat allergy is estimated to be at least 1 percent of the population. Ticks are not new. Neither is the human consumption of meat. Why the sudden problem for so many? One possibility is that the ticks have changed somehow.
The idea is plausible and could nicely explain how an arachnid that has been around for a long time could begin causing a new set of complications. Scientists have long debated where the alpha-gal in the tick originates: Does it come from the blood a tick sucks from other mammals and then regurgitates as it feeds on people, or does it come from the tick itself? Shahid Karim, a vector biologist at the University of Southern Mississippi, in Hattiesburg, told me that the answer might be neither; the sugar probably comes from the microbes that the tick carries within it. So it’s entirely possible, he said, that changes in its microbiome could, by increasing the amount of alpha-gal humans are exposed to in tick bites, make the lone-star tick more likely to induce meat allergy.
What such an account fails to address, however, is why the meat allergy has increased in other parts of the world, like Australia and Europe. (Van Nunen says that in the tick country around Sydney, people are now more likely to carry EpiPens, which contain a shot of adrenaline, for meat allergy than for better-known peanut allergies.) Other tick species are linked with meat allergy in those regions, not the lone-star tick. And it seems very unlikely that the microbiomes of all these ticks on different continents have changed in similar ways at the same time.
“I don’t for the life of me have a unifying hypothesis for why it’s happening everywhere,” Commins told me, although he added that pesticides could be one factor changing tick microbiomes globally.
It may simply be that an increase in the number of ticks has turned a problem once so rare that it went scientifically unnoticed into an observable epidemic.
“I think we’ve got far more tick bites today than people had as recently as 35 years ago,” Platts-Mills told me. He lays the blame for the growing spread of ticks on newly abundant deer.
In Virginia, he thinks new laws requiring dogs to remain on leashes have emboldened deer, which then bring ticks closer to people. People aren’t necessarily venturing deeper into the forests than in the past, he says. More than half the patients he sees with the allergy were bitten on their own lawns.
His leash theory is anecdotal, but it’s certainly true that the current ecological state of Eastern forests is probably encouraging ticks to multiply. After having been cleared in the Colonial era, the forests have partly grown back. Deer and turkey, which the lone-star tick likes to feed on, are abundant again. They thrive in the new-growth forests, now fragmented by roads and suburbs. Large predators are mostly absent. And the rise of tick-borne disease generally has been linked with the decline (or absence) of predators that eat the animals ticks feed on. In Australia, for example, van Nunen points to the eradication of foxes, an introduced species there, as one factor in the increase of ticks and the rise of meat allergy.
We might label this the disturbed ecosystem theory of meat allergy. Forests ecosystems have recovered partially — lots of animal hosts for ticks but not enough predators to keep those hosts in check — and this imbalance has fostered an exponential growth in the number of ticks. In some ways, this is the most probable explanation for the rise of meat allergy. Climate change may be aiding the lone-star tick’s move northward too, Rick Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies, told me. Hundreds of cases of meat allergy have been diagnosed on Long Island in recent years, which wasn’t part of the tick’s range in recent history. The tick has been spotted as far north as Maine.
But what’s happening in the American East can’t account for the full extent of the phenomenon elsewhere in the world. In Northern Europe, ticks are proliferating as forests recover and the climate becomes warmer. But in Spain and Southern Europe, the rising incidence of meat allergy has not been accompanied by an increase in tick numbers, according to José de la Fuente, a professor at the Institute of Game and Wildlife Research in Ciudad Real, Spain. For him, the mystery of meat allergy is captured in one question: If a tick bites two genetically similar people, why might only one develop the meat allergy?
Onyinye Iweala, an assistant professor who works with Scott Commins’s lab at the University of North Carolina, echoes this uncertainty. Why are some people sensitized to alpha-gal — meaning they have allergic antibodies directed at the sugar in their blood stream — but never have an allergic reaction to it? This can happen in all allergies. You can have antibodies to, say, cat dander, yet never wheeze or sneeze around cats. Iweala suspects that sensitization to alpha-gal isn’t new. What’s changing is the proportion of people who, after sensitization, proceed to overt allergy. Something else in the environment, she told me, is likely pushing people toward full-blown meat allergy. Perhaps shifts in the microbes that live within us have somehow made us more easily sensitized by tick bite. As a model of how this might work, Iweala points to intriguing research on the interaction between malaria and the human microbiome that centers on alpha-gal.
OUR DISTANT ANCESTORS once made alpha-gal. Understanding why humans don’t could shed light on the meat-allergy mystery. Like other mammals, South American monkeys produce alpha-gal. Only Old World monkeys and apes (and humans) have lost the ability to make the sugar. Hence scientists deduce that the change most likely happened after New and Old World primates diverged from each other around 40 million years ago. One explanation for the disappearance of alpha-gal is that it was driven by some catastrophe, a deadly infection that afflicted Old World primates, perhaps, and as a result maybe these distant relatives of ours stopped being able to produce the sugar because doing so conferred an evolutionary advantage. The mutation that eliminated alpha-gal could have improved a primate’s ability to fight off an infection by enabling its immune system to more easily distinguish between its own body and some pathogen with alpha-gal.
What could this pathogen have been? In the late 2000s, Miguel Soares, a scientist at the Instituto Gulbenkian de Ciência in Oeiras, Portugal, began to suspect the plasmodium parasite that causes malaria. Because the protozoan is so deadly and has historically been so widespread in warmer climes, geneticists often say that malaria has been the single greatest force shaping the human genome in our recent evolutionary history. The parasite remains a leading cause of death in the developing world. And it’s coated in alpha-gal.
Soares and his colleagues investigated a rural Malian population that was naturally exposed to malaria. As it happens, humans produce some antibodies to alpha-gal all the time. They’re not allergic antibodies like those responsible for Lee Niegelsky’s anaphylactic experience, but antimicrobial ones that give rise to a different, less drastic immune response. Between 1 and 5 percent of all the antibodies circulating in any person, a remarkably large quantity, are directed at alpha-gal, Soares estimates. The target of these antibodies is not the alpha-gal in the steak you may have eaten for dinner but the alpha-gal that leaks into circulation from the microbes dwelling in your gut. There are natural variations in the amount of these antibodies any individual produces; some people make more, some less. Soares wanted to know if this variability influenced the villagers’ susceptibility to malaria.
What was different about those with more alpha-gal antibodies? They had more gut microbes that produced the sugar, Soares speculated. By priming their immune response against alpha-gal, these individuals’ microbiomes probably helped shield them against malaria. Soares showed as much using mice. Rodents colonized by a strain of E. coli found in the human microbiome that contains alpha-gal produced antibodies to the sugar and were protected from malaria. Rodents that harbored an E. coli strain that didn’t produce the sugar, on the other hand, were not protected. (Other scientists later observed a connection between resistance to malaria and the composition of Malian villagers’ microbiomes.) This research highlights one reason we probably have a few pounds of microbes in us: Friendly microbes can help protect us against unfriendly ones.
Soares is currently working on a vaccine to spur the immune system to attack alpha-gal more actively, thereby conferring greater protection against malaria. His findings also raise the prospect, at least theoretically, of an antimalarial probiotic. In the context of meat allergy, his work underscores the fact that our microbes may affect how we respond to alpha-gal from other sources, including, perhaps, tick bites.
How might this work? You can envision antibodies as arrows that have Velcro on the front instead of arrowheads. Depending on their targets, that Velcro sticks only to a particular substance, like alpha-gal or peanut protein. The back end of the arrow displays a signal that tells the immune system what to do. Allergic antibodies, called immunoglobulin-E, or IgE for short, call for an allergic response. But the antibodies that humans typically have in circulation directed at alpha-gal are antimicrobial antibodies like IgM and IgG, not allergic ones.
A question central to the meat-allergy mystery is how, if we’re always exposed to alpha-gal from our gut microbes, and we’re constantly mounting a nonallergic response against it, the lone-star tick prompts what’s called “class switching,” spurring the immune system to pump out allergic antibodies instead of antimicrobial ones?
The microbes we host may, by stimulating the immune system and guiding its response to alpha-gal, make this class switching more or less likely, Onyinye Iweala told me. But scientists don’t yet know how the relationship works. Perhaps if your microbiota have more species that produce alpha-gal, these microbes stimulate your immune system in a way that protects you from allergic sensitization to the sugar when a tick bites. Or maybe the relationship works the other way around: If you host fewer alpha-gal-producing species and your immune system is less exposed to alpha-gal on a daily basis, that relative lack of stimulation might prevent alpha-gal allergy from developing when you’re bitten by a tick. These interactions can be tested — as Iweala is doing — with mice that, like humans, don’t produce alpha-gal.
What scientists do know is that if you treat a baboon with antibiotics, reducing the amount of alpha-gal-producing microbes in its gut, and thus lessening the stimulation they provide, the quantity of alpha-gal antibodies in its bloodstream also declines. This suggests that altering a primate’s gut microbes may change its immune response to alpha-gal. People living in developed countries, where most cases of meat allergy have been diagnosed, have been doing something very similar to themselves. “We keep changing the microbiome with antibiotics and what we eat,” Iweala says. By tweaking the microbes that live inside us, we may have inadvertently changed how our immune system responds to alpha-gal, making us more vulnerable to tick-induced meat allergy. It’s also possible, however, that the microbes that determine the general tone of our immune function have shifted, altering how we respond to all potential allergens, not just alpha-gal.
Since at least the late 20th century, and probably earlier, we’ve been living in the midst of what’s often called the allergy epidemic, an era that has seen an increase in the prevalence and severity of food allergies generally and, before that, a rise in the prevalence of respiratory allergies and asthma. The forces driving this trend may help account for meat allergy as well. A leading explanation holds that we develop more allergies now because our immune systems have become more sensitive to what they encounter, not because they are exposed to more pollens or allergenic foods than in the past. The reason the modern immune system errs this way, the thinking goes, is that it’s not receiving the right kind of education.
The news media have taken to calling this explanation the “hygiene hypothesis,” which is unfortunate and misleading; personal hygiene has little to do with what’s at issue. More accurate terms coined by researchers include the microbial-deprivation hypothesis, the disappearing-microbiota hypothesis and even the “old friends” hypothesis (the implication being that we’ve lost contact with once-ever-present friendly organisms).
Whatever you call it, the idea is that the rising tide of allergic diseases comes from changes to the type and quantity of microbes we encounter in our environment, particularly in our early life, as well as from changes to the microbes that live on and in us. Improved sanitation, antibiotics and the junk-food-ification of our diet, among other factors, may have shifted our microbial communities, giving us an immune system that’s overly jumpy, unable to reliably distinguish friend from foe and prone to diseases of overreaction, like allergies.
Studies on populations that have bucked the increase in allergies support the idea. Nearly 20 years of research on European children who grow up on farms with animals, for example, indicates that they are less likely to have respiratory allergies, asthma and eczema compared with other children in the same rural areas. The abundant microbial stimulation of the farm environment, scientists have proposed, tunes farming children’s immune system in a way that prevents allergic disease. The cowshed has thus become a stand-in for premodern conditions and the immune system that that environment produces — lightly stimulated but less likely to react to allergens — a model of how the human immune system might have worked in a more microbially enriched past.
So here is the question as it relates to meat allergy: If a lone-star tick bit a Bavarian farm-raised child, would she be less likely to develop an allergy to alpha-gal compared with her nonfarming counterparts? Put another way, if the tick bit someone 150 years ago when the whole world was more like a cowshed, would that person be less or more likely to develop a food allergy than someone from modern-day Chapel Hill?
It’s pure speculation at this point, but gradual, intergenerational changes to our microbes may have altered our immunological tenor, shifting it from cool, calm and collected toward restless and irritable and increasing the odds of developing allergy from a tick bite. Today we may encounter more ticks than in times past, but they may also be interacting with an immune system that’s more sensitive to their bites than ever before. “It’s the ‘perfect storm,’ as you would say in America,” Sheryl van Nunen told me.
For Lee Niegelsky, who had eaten hamburgers his entire life, the allergy forced him to constantly scrutinize his diet. You don’t realize how many foods have meat-derived products in them, he told me — especially in the South, where pork fat and bacon are widely used as flavoring — until you have to avoid meat for fear of passing out. Not long ago, for example, he fell ill after eating clam chowder, which he attributes to meat broth that he suspects was in the soup.
The good news is that, provided you’re not bitten by a tick again, sometimes the meat allergy fades on its own. A year after his visit to the emergency room, under Scott Commin’s supervision, Niegelsky began introducing small amounts of lean meat into his diet. The idea is to test the possibility that his allergic alpha-gal antibodies have subsided to the point that his immune system no longer attacks the sugar. It took Niegelsky about a week to muster the courage to take his first bite of pork tenderloin. He waited anxiously for six hours. When nothing happened, he moved on to steak.
“According to Dr. Nicolson, some of the experiments used Mycoplasma while others utilized various “cocktails of microbial agents” such as Mycoplasma, Brucella, and DNA viruses such as Parvovirus B19. This project later become the topic of a book by Dr. Nicolson entitled Project Day Lily.
Dr. Nicolson believes that Mycoplasma fermentans is a naturally occurring microbe. However, some of the strains that exist today have been weaponized. Dr. Nicolson’s research found unusual genes in M. fermentans incognitus that were consistent with a weaponized form of the organism. Weaponzing of an organism is done in an attempt to make a germ more pathogenic, immunosuppressive, resistant to heat and dryness, and to increase its survival rate such that the germ could be used in various types of weapons. Genes which were part of the HIV‐1 envelope gene were found in these Mycoplasma. This means that the infection may not give someone HIV, but that it may result in some of the debilitating symptoms of the HIV disease.”
Regarding the weaponization of tick pathogens: https://www.lymedisease.org/lymepolicywonk-questioning-governments-role-lyme-disease-make-conspiracy-theorist/ (Go here to read excerpts of an interview with a biologist who acknowledged doing biowarfare work on ticks and mosquitoes. He admits every time he has a strange illness his physician says it’s probably a rickettsia – an idiopathic condition that never tests positive but symptoms indicate it.)
‘The interview suggests to me that the reason we have such a large problem with our tick population today may be related to military experiments in the 50s. They were part of a biological warfare effort against the Russians. One goal was to figure out how to get ticks to reproduce quickly and abundantly, as well as how to distribute ticks to targeted areas.”
For a lengthy but informative read on the Lyme-Biowarfare connections: CitizensAlert_Bob13 (Scroll to page 44 to see an executive summary. Please notice the names of Steere, Barbour, Shapiro, Klempner, and Wormser, the first four are affiliated with the CDC Epidemic Intelligence Service (EIS). Wormser, lead author of the fraudulent Lyme treatment guidelines, lectures as an expert on biowarefare agents and treatments). The author of the pdf believes borrelia (Lyme) has been bioweaponized due to (excerpt from pdf footnote):
So you tell me. Could all this lab tweaking have something to do with tick borne illness and allergies?
AUTHOR: MEGAN MOLTENIMEGAN MOLTENI
WHEN RICK OSTFELD gets bitten by a tick, he knows right away. After decades studying tick-borne diseases as an ecologist at the Cary Institute of Ecosystem Studies in Millbrook, New York, Ostfeld has been bitten more than 100 times, and his body now reacts to tick saliva with an intense burning sensation. He’s an exception. Most people don’t even notice that they’ve been bitten until after the pest has had time to suck up a blood meal and transfer any infections it has circulating in its spit.
Around the world, diseases spread by ticks are on the rise. Reported cases of Lyme, the most common US tick-borne illness, have quadrupled since the 1990s. Other life-threatening infections like anaplasmosis, babesiosis, and Rocky Mountain spotted fever are increasing in incidence even more quickly than Lyme. Meat allergies caused by tick bites have skyrocketed from a few dozen a decade ago to more than 5,000 in the US alone, according to experts. And new tick-borne pathogens are emerging at a troubling clip; since 2004, seven new viruses and bugs transmitted through tick bite have shown up in humans in the US.
Scientists don’t know exactly which combination of factors—shifting climate patterns, human sprawl, deforestation—is leading to more ticks in more places. But there’s no denying the recent population explosion, especially of the species that carries Lyme disease: the black-legged tick.
“Whole new communities are being engulfed by this tick every year,” says Ostfeld. “And that means more people getting sick.”
Tick science, surveillance, and management efforts have so far not kept pace. But the country’s increasingly dire tick-borne disease burden has begun to galvanize a groundswell of research interest and funding.
In 1942, Congress established the CDC specifically to prevent malaria, a public health crisis spreading through mosquitoes. Which is why many US states and counties today still have active surveillance programs for skeeters. The Centers for Disease Control and Prevention uses data from these government entities to regularly update distribution maps, track emerging threats (like Zika), and coordinate control efforts. No such system exists for ticks.
Public health departments are required to report back to the CDC on Lyme and six other tick-borne infections. Those cases combined with county-level surveys and some published academic studies make up the bulk of what the agency knows about national tick distribution. But this data, patchy and stuck in time, doesn’t do a lot to help public health officials on the ground.
“We’ve got national maps, but we don’t have detailed local information about where the worst areas for ticks are located,” says Ben Beard, chief of the CDC’s bacterial diseases branch in the division of vector-borne diseases. “The reason for that is there has never been public funding to support systematic tick surveillance efforts.”
That’s something Beard is trying to change. He says the CDC is currently in the process of organizing a nationwide surveillance program, which could launch within the year. It will pull data collected by state health departments and the CDC’s five regional centers about tick prevalence and the pathogens they’re carrying to build a better picture of where outbreaks and hot spots are developing, especially on the expanding edge of tick populations.
The CDC is also a few years into a massive nationwide study it’s conducting with the Mayo Clinic, which will eventually enroll 30,000 people who’ve been bitten by ticks. Each one will be tested for known tick diseases, and next-generation sequencing conducted at CDC will screen for any other pathogens that might be present. Together with patient data, it should provide a more detailed picture of exactly what’s out there.
Together, these efforts are helping to change the way people and government agencies think about ticks as a public health threat.
“Responsibility for tick control has always fallen to individuals and homeowners,” says Beard. “It’s not been seen as an official civic duty, but we think it’s time whole communities got engaged. And getting better tick surveillance data will help us define risk for these communities in areas where people aren’t used to looking for tick-borne diseases.”
The trouble is that scientists also know very little about which interventions actually reduce those risks.
“There’s no shortage of products to control ticks,” says Ostfeld. “But it’s never been demonstrated that they do a good enough job, deployed in the right places, to prevent any cases of tick-borne disease.”
In a double-blind trial published in 2016, CDC researchers treated some yards with insecticides and others with a placebo. The treated yards knocked back tick numbers by 63 percent, but families living in the treated homes were still just as likely to be diagnosed with Lyme.
Ostfeld and his wife and research partner Felicia Keesing are in the middle of a four-year study to evaluate the efficacy of two tick-control methods in their home territory of Dutchess County, an area with one of the country’s highest rates of Lyme disease. It’s a private-public partnership between their academic institutions, the CDC, and the Steven and Alexandra Cohen Foundation, which provided a $5 million grant.
Ostfeld and Keesing are blanketing entire neighborhoods in either a natural fungus-based spray or tick boxes, or both. The tick boxes attract small mammal hosts, which get a splash of tick-killing chemicals when they venture inside. They check with all the human participants every two weeks for 10 months of the year to see if anyone’s gotten sick. By the end of 2020 the study should be able to tell them how well these methods, used together or separately on a neighborhood-wide scale, can reduce the risk of Lyme.
“If we get a definitive answer that these work the next task would be to figure out how to make such a program more broadly available. Who’s going to pay for it, who’s going to coordinate it?” says Ostfeld. “If it doesn’t work then perhaps the conclusion is maybe environmental control just can’t be done.”
In that case, people would be stuck with pretty much the same options they have today: protective clothing, repellants, and daily partner tick-checks. It’s better than nothing. But with more and more people getting sick, the US will need better solutions soon.
Great article pointing out the scary fact that only 6 pathogens transmitted by ticks are being reported on. There are currently 18 pathogens and counting…..so the numbers are woefully inadequate.
Colorado Tick Fever
Crimean-Congo hemorrhagic Fever
Meat Allergy/Alpha Gal
Pacific Coast Tick Fever: Richettsia philipii
Rickettsia parkeri Richettsiosis
Rocky Mountain Spotted Fever
STARI: Southern Tick-Associated Rash Illness
June 14, 2018 Josh Barney, firstname.lastname@example.org
University of Virginia School of Medicine researchers have linked sensitivity to an allergen in red meat – a sensitivity spread by tick bites – with a buildup of fatty plaque in the arteries of the heart. This buildup may increase the risk of heart attacks and stroke.
The bite of the lone star tick can cause people to develop an allergic reaction to red meat. However, many people who do not exhibit symptoms of the allergy are still sensitive to the allergen found in meat. UVA’s new study linked sensitivity to the allergen with the increased plaque buildup, as measured by a blood test.
The research team drew from both allergists and cardiologists, and included, from left, Dr. Thomas Platts-Mills, Dr. Coleen McNamara, Dr. Jeff Wilson and Anh Nguyen. (Photo by Dan Addison, University Communications)
“This novel finding from a small group of subjects examined at the University of Virginia raises the intriguing possibility that asymptomatic allergy to red meat may be an under-recognized factor in heart disease,” said study leader Dr. Coleen McNamara of UVA’s Robert M. Berne Cardiovascular Research Center and UVA’s Division of Cardiovascular Medicine. “These preliminary findings underscore the need for further clinical studies in larger populations from diverse geographic regions.”
Looking at 118 patients, the researchers determined that those sensitive to the meat allergen had 30 percent more plaque accumulation inside their arteries than those without the sensitivity. Further, a higher percentage of the plaques had features characteristic of unstable plaques that are more likely to cause heart attacks.
With the meat allergy, people become sensitized to alpha-gal, a type of sugar found in red meat. People with the symptomatic form of the allergy can develop hives, stomach upset, have trouble breathing or exhibit other symptoms three to eight hours after consuming meat from mammals. (Poultry and fish do not trigger a reaction.)
What’s it like to develop a meat allergy? https://makingofmedicine.virginia.edu/2018/03/29/the-meat-allergy-whats-it-like/
Other people can be sensitive to alpha-gal and not develop symptoms. In fact, far more people are thought to be in this latter group. For example, up to 20 percent of people in Central Virginia and other parts of the Southeast may be sensitized to alpha-gal, but not show symptoms.
The allergy to alpha-gal was first reported in 2009 by Dr. Thomas Platts-Mills, who heads UVA’s Division of Allergy and Clinical Immunology, and his colleague Dr. Scott Commins. Since then, there have been increasing numbers of cases of the meat allergy reported across the U.S., especially as the lone star tick’s territory grows. Previously found predominantly in the Southeast, the tick has now spread west and north, all the way into Canada.
UVA’s new study suggests that doctors could develop a blood test to benefit people sensitive to the allergen.
“This work raises the possibility that in the future a blood test could help predict individuals, even those without symptoms of red meat allergy, who might benefit from avoiding red meat. However, at the moment, red meat avoidance is only indicated for those with allergic symptoms,” said researcher Dr. Jeff Wilson of UVA’s allergy division.
The work represents a significant collaboration between allergy and cardiology experts at UVA. The researchers have published their findings in Arteriosclerosis, Thrombosis and Vascular Biology, a journal of the American Heart Association. The research team consisted of Wilson, Anh Nguyen, Alexander Schuyler, Commins, Angela Taylor, Platts-Mills and McNamara.
The work was supported by the National Institutes of Health, grants KO8-AI085190, K23-HL093118, RO1-AI 20565, PO1-HL55798, RO1-HL136098-01 and RO1-HL107490.
UVA Health System