What ticks actually do to your body, from Lyme to alpha-gal

Short answer

Three things, mechanically: they infect you, they poison you, or they rewire your immune system. Lyme is by far the most common, roughly hundreds of thousands of US cases a year, and a deer tick generally has to stay attached 36 to 48 hours to transmit it. Powassan virus can transmit in 15 minutes and kills about 10% of people sick enough to be hospitalized, but only 30 cases have been reported in 2026 and 76 last year. Alpha-gal syndrome, the tick-induced red meat allergy, shows 24% antibody seroprevalence in blood donors across five southern states against roughly 500 diagnosed cases a year.

I live in Connecticut, a few miles from the town that gave Lyme disease its name. So I have opinions about ticks. Most of them are unfavorable.

Let's start with a correction I owe the entomologists. Ticks are not bugs. They are not even insects. They are arachnids, more closely related to spiders than to mosquitoes. That fact will not make you feel better about finding one on your leg.

There are dozens of tick-borne illnesses, and I could talk about all of them, but the useful way to think about ticks is not as a list of diseases. It's as three mechanisms. A tick can infect you with something. A tick can poison you. And a tick can rewire your immune system.

Why the tiny ones are the dangerous ones

Ticks need blood to advance through their life cycle. Not just to grow, the way anything needs food to grow. Each stage, larva to nymph to adult, requires a blood meal to unlock the next one. They level up by feeding on you. Then they drop off, molt, and wait for the next host. A fully engorged tick can reach something like 600 times its starting weight, which is as unpleasant to look at as it sounds.

The stage that matters most for human disease is the nymph. Not because nymphs are uniquely infected, but because they're the size of a poppy seed. A black speck in your hair. You will not see it.

How likely is that speck to be carrying something? For deer ticks, roughly 25% of nymphs and 50% of adults test positive for the Lyme bacterium. If you find a deer tick on you, the odds are decent it was carrying Lyme.

Infection: Lyme is common, Powassan is terrifying and rare

Lyme disease starts with a spirochete, a spiral-shaped bacterium in the same general family as syphilis. It's called Borrelia burgdorferi, named for Willy Burgdorfer, who identified it. The tick has to feed for a while before it transmits, because the process involves the tick metabolizing some of your blood and putting it back into you. That takes time. Somewhere in the range of 36 to 48 hours. You have a real window to find and remove the tick.

Now consider Powassan virus, carried by the same black-legged deer tick. Transmission takes about 15 minutes. You can miss a tick for two days. You can definitely miss one for fifteen minutes.

Google Powassan and you'll find that it has no treatment and a 10% case fatality rate. Both of those are technically true and together they are badly misleading. What the virus does in most people is nothing. In a small number of people it causes meningitis, and those people are hospitalized, very sick, and get supportive care because antibiotics don't work on viruses. Among that group, about one in ten dies.

The numbers put it in perspective. Thirty cases so far in 2026. Seventy-six last year. In a country of 330 million people, with tens of millions living in the Northeast. And serosurveys, which look for antibody evidence of past exposure, suggest far more people have encountered this virus than have ever been sick from it.

People are bad at small probabilities. A 10% fatality rate lodges in your head and stays there, and the 76-out-of-everyone part doesn't. You are considerably more likely to die driving to the trailhead than from anything you pick up in the woods. The health benefit of the hike almost certainly wins. If Powassan motivates you to do a tick check, fine. Don't let it keep you up at night.

Other infections are worth knowing about. Babesiosis is a parasite that invades red blood cells, the closest thing we have in the United States to malaria. It's a different organism, but the mechanism and the presentation are similar: severe anemia, and patients who look like the malaria cases you learned about in medical school. We see it in Connecticut hospitals. Roughly 100 to 500 cases a year nationally, so my interest in it says more about my referral pattern than about your risk. Babesiosis often causes kidney dysfunction, which is how a nephrologist ends up at the bedside.

Poison: the paralysis that reverses when you pull the tick off

Some ticks carry a neurotoxin in their saliva. No infection involved. The toxin causes a flaccid, ascending paralysis: weakness that starts in the legs and moves up the body. If you're a clinician and you see that pattern, your first thought is Guillain-Barré syndrome, because it looks exactly the same.

Except sometimes it's a tick. And if you find the tick and remove it, the paralysis resolves within hours.

That's the practical point for anyone working up a patient with an ascending paralysis: do a thorough tick check. Check the scalp. Check everywhere. It's one of the few times in medicine where the cure is a pair of tweezers.

Immune rewiring: alpha-gal and the red meat allergy

A recurring theme in allergy is that you tend to become allergic to things that enter your body the wrong way. Eat a substance and your immune system usually tolerates it. Inject it under the skin and the rules change.

Every mammalian species carries a sugar on its cell surfaces called galactose-alpha-1,3-galactose. Every one except the old world primates. Somewhere in our evolutionary history, humans, chimpanzees, and gorillas lost the gene. We don't make it. We do eat it constantly, in beef and pork and lamb, and that's fine, because it goes through the GI tract.

The lone star tick has alpha-gal in its saliva. When it bites you, it injects the sugar directly into your skin. Some people then develop an IgE allergy to it, and from that point on, mammalian meat is a problem.

The allergy behaves oddly. It's usually not immediate anaphylaxis. Symptoms show up hours after the meal, presumably because the offending sugar has to be digested and absorbed first. And the presenting complaints are frequently gastrointestinal: pain, bloating, diarrhea, sometimes vomiting. Because the gap between eating and getting sick is so long, it often doesn't occur to anyone that this is an allergy at all.

Here's where it gets interesting. Testing suggests exposure is enormously more common than disease. In roughly 3,000 residual blood donor samples from 2024 to 2025, estimated alpha-gal IgE seroprevalence was 24% across the five highest states: Arkansas, Kentucky, Missouri, Tennessee, and Virginia. Against about 500 diagnosed cases a year. Twenty-four percent of the people in those states are not allergic to meat. An antibody titer is not the same thing as a clinical immune reaction.

For most people who do develop symptoms, the allergy fades over time if they avoid further tick bites. For some, it doesn't, and they never eat meat again.

Lyme disease: what it does and how it's diagnosed

Lyme is the most common tick-borne disease in the United States. The exact annual case count isn't clear, but it's in the hundreds of thousands.

The origin story matters, and not just as history. In the mid-1970s, a group of mothers in Old Lyme, Connecticut noticed that an implausible number of local children had been diagnosed with juvenile rheumatoid arthritis. That's not a common disease and it does not cluster. They pushed. They kept pushing. Eventually researchers at Yale took them seriously, worked it up, and found the spirochete.

So Lyme begins with patients being disbelieved and physicians eventually catching up. Hold onto that, because it explains a great deal about where the field is now.

Clinically, the standard framing splits Lyme into early localized and late disseminated disease. Early localized is the rash, erythema migrans, the classic bullseye. Plus flu-like symptoms: fatigue, headache, aches. This is when you want to treat.

The rash is less obvious in real life than in the textbook photos. My own daughter had Lyme. I photographed a vague ring-shaped thing on her back, sent it to a pediatrician, and was told it didn't really look like erythema migrans. Too faint. She had Lyme. And roughly 70% to 80% of Lyme cases produce the rash, which means one in four or five don't. You can have Lyme with no rash at all.

Untreated, the infection disseminates. Joints, classically. My daughter ended up diagnosed because of a large effusion in her knee. You can also get cardiac abnormalities, and facial palsy is fairly common, which can look alarmingly like a stroke. Nearly all of it improves with treatment.

If you have a tick bite and a bullseye rash, you don't need a test. You get doxycycline. Several doses of doxycycline, to be clear, not one pill. Some clinicians will test anyway to document it, but the test is most likely to be falsely negative early, before you've built an antibody response, which is precisely when you want the antibiotic on board.

Some pediatricians recommend a single prophylactic dose of doxycycline for any tick bite. The randomized evidence for that is thin. It rests essentially on one trial from 2001 in which erythema migrans was the outcome, with 1 of 235 in the treated group versus 8 of 247 in the comparison group. You may hear the recommendation. Know what it's built on.

Testing gets harder in the ambiguous case: no remembered bite, no rash, and then weeks later a facial palsy or nerve pain or a scattering of odd symptoms. Standard testing looks for antibodies to the spirochete, and the FDA and CDC recommend a two-tiered approach. A sensitive first test that picks up nearly everything, then a more specific confirmatory test. Run in a certified lab, that combination detects something like 80% of true infections with a false positive rate around 10%. Not perfect. Not bad. It can miss you early, and it can flag an infection you cleared years ago, because antibodies persist.

Then there is the parallel testing world. An entire ecosystem of unlicensed labs runs research-grade assays with detection thresholds set very low and substantial cross-reactivity, producing false positive rates north of 50%. That ecosystem exists for a reason, and the reason is that patients were not being listened to.

Chronic Lyme, and why the term causes so much trouble

Definitions first, because people mean different things.

Late disseminated Lyme disease is untreated infection that has spread. Joints, heart, nerves. You have technically had it a long time, but that is not what anyone means by chronic Lyme.

Post-treatment Lyme disease syndrome is what it sounds like. Documented Lyme, treated appropriately, and you're still sick. That's not how bacterial infections are supposed to work, and yet it happens. In one analysis, persistent symptoms were reported in 6% of patients who presented with erythema migrans versus 21% of those with disseminated disease.

Chronic Lyme is a much bigger tent. It includes post-treatment Lyme disease syndrome, and it also includes a far larger group of people with long-term symptoms and no documented infection, sometimes no known tick bite at all.

The symptom list is the problem: fatigue, brain fog, joint pain, intermittent rashes, GI distress, depression, mania, psychosis. These can be genuinely debilitating. I have seen people unable to walk. They are also symptoms produced by a long list of other conditions, and there is no clear diagnostic test for either syndrome.

A loose case definition feels generous and is scientifically corrosive. The same thing happened with long COVID. Everyone wanted a big tent, so the definition covered fatigue, and postural tachycardia, and brain fog, and nearly anything else, and then when researchers looked for biomarkers separating cases from controls they found nothing, because the cases were not one group. Sometimes you want a definition so tight it excludes people, precisely so you can identify the biology, build a test, and then widen the tent on solid ground.

What happens instead is that patients with vague symptoms and no answers get funneled, usually via social media, toward self-described "Lyme literate" practitioners. That phrase is too broad to be useful. I know excellent infectious disease physicians in Connecticut who would happily call themselves Lyme literate and who know every entry in my very long table of tick-borne illnesses. There is also a more shadowy medical-adjacent world where the practitioners refer to one another, send blood to a specific set of labs that often lack FDA clearance and sometimes lack CLIA certification, and reliably get positive results back. I have watched patients enter that pipeline with vague symptoms, receive a confirmatory-looking test, and start down a treatment path.

That path frequently ends in months of high-dose intravenous antibiotics. It has been tested repeatedly and it does not work. The PLEASE trial randomized 281 patients, 89% previously treated, to 14 days of IV ceftriaxone followed by 12 weeks of doxycycline, clarithromycin plus hydroxychloroquine, or placebo. At 52 weeks there was no difference in health-related quality of life. That is not the only trial. It is one of several.

And the harms are not theoretical. Long-term IV antibiotics require an indwelling catheter, a PICC or a central line, which is a permanent breach in your skin and a direct route for bacteria into your bloodstream. Months of antibiotics raise your risk of C. difficile colitis, because you have wiped out the gut flora holding it in check. They raise your risk of candida, because yeast is unbothered by antibacterials, and candida in the bloodstream of someone with an indwelling line is life-threatening. If a practitioner reaches the point of proposing a line and several months of infusions, get a second opinion. I mean that as a hard rule.

Two other things to watch for. People will tell you the treatment worked, and the placebo effect is genuinely powerful, which is exactly why randomized data matter more here, not less, when the intervention carries this much risk. And when patients feel worse on antibiotics, the response in some circles is to call it a Jarisch-Herxheimer reaction, or "herxing." That reaction is real. Kill a large load of spirochetes, in syphilis classically or in acute Lyme, and the dying organisms release inflammatory material that can produce about 24 hours of fever and chills. But in chronic Lyme we cannot isolate the bacteria. There's nothing there to lyse. So any improvement confirms the treatment and any deterioration also confirms the treatment, and the loop never breaks. Watch, too, whether the practitioner takes insurance. These infusions run into the thousands of dollars, repeated over months, and I have seen it become financially devastating.

The bioweapon story, and why it doesn't hold

You may have heard that Lyme is the product of gain-of-function research or an escaped bioweapon. The Secretary of Health and Human Services has said so.

The story traces to a 2004 book called Lab 257, about the Plum Island Animal Disease Center on the eastern tip of Long Island. Plum Island is real, it studies animal diseases including some tick-borne ones, and Lyme, Connecticut sits across the sound. That's the whole geographic argument. There's no evidence of Lyme experiments there. The other thread is that Willy Burgdorfer, who identified the spirochete, worked at Rocky Mountain Labs, which did run an entomological warfare program. The government was interested in whether insects could spread disease. So a scientist who was an expert in tick-borne disease worked on a program about tick-borne disease. That is what staffing looks like.

Two pieces of evidence kill the theory outright. First, the timeline. Lyme was identified in the 1970s, and those programs date to the 1960s, but the bacterium substantially predates both. We have direct evidence of Borrelia burgdorferi in white-footed mice from museum specimens going back to at least 1898.

Second, genetics. If the organism had been released at a single point in time and place, say Lyme, Connecticut in 1970, its descendants fifty years later would be highly genetically similar to one another. Instead Borrelia burgdorferi is strikingly diverse, and the methods used to date that diversity put its lineage in mammals back millions of years.

Also, as a matter of engineering, a tick is a terrible delivery vehicle. It crawls. It has to stay attached for two days. Mosquitoes fly to you and bite immediately. Whoever picked the crawler had one job.

The appeal of these stories isn't really about ticks. People want explanations. "Animals carry diseases and sometimes you catch them" is unsatisfying in a way that "someone did this on purpose" is not, because malfeasance implies someone could have stopped it, and could stop it next time. And Lyme lends itself to that framing better than most diseases, because its origin story genuinely is one of people being dismissed.

Prevention, and a vaccine that may finally return

Permethrin, which comes in a spray bottle, goes on your clothing, not your skin. If you're hiking in tick country, spray your clothes. DEET works too, it isn't poison, and it covers you for mosquitoes at the same time. Then check yourself, and check each other. It won't help with Powassan's 15-minute window, but for Lyme, pulling ticks off within a day or two is genuinely protective.

As for a vaccine: we used to have one. LYMErix came off the market in 2002 amid litigation and claims of autoimmune side effects. It worked. It also, I suspect, didn't sell well enough.

My dog gets a Lyme vaccine. You can't. That may change. The VALOR trial, with 9,437 participants, completed in March and reported 73.2% efficacy against infection. The confidence interval runs from 15.8% to 93.5%, which is enormous, because there were very few cases. So the point estimate is encouraging and the precision is poor. More cases would tighten it.

Bottom line

Ticks are worth avoiding and not worth panicking about. Powassan is genuinely frightening and genuinely rare. Alpha-gal is far more often an antibody finding than a disease. Lyme, caught early with a rash, is a straightforward course of doxycycline and it works.

The hard part is what comes after. Post-treatment Lyme disease syndrome is real, and we have no test for it, no tight case definition, and no proven therapy. Long-term IV antibiotics have failed in multiple randomized trials and carry real risk of sepsis, C. difficile, and candidemia. Saying that is not the same as telling patients their symptoms are imaginary, and physicians who conflate the two are the reason the alternative ecosystem thrives.

I know how it feels from the other side of the exam table. A patient comes in, I run the tests, nothing turns up, and I have nothing to offer. That's miserable. It's also exactly where research is most needed. HHS recently announced new initiatives on Lyme, including funding aimed at these long-term post-treatment syndromes, which is the right target. Until that work is done, people in distress will keep being offered solutions, and I don't want to talk anyone out of exploring options, with the single exception of months of intravenous antibiotics, because that one can kill you. Everything else comes down to listening, working symptom by symptom, and getting patients to the right specialists.

Here's our discussion from the episode:

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