Dr. Ben Reebs: On today’s episode of the Modern Vital Podcast. We’re going to talk a little bit about how tick borne disease can trigger autoimmune disease. Tick borne disease is also known as TBD and autoimmune disease is also known as AD. Our modern vital fact of the day is that the main mechanism associated with tick borne diseases and autoimmune diseases is called molecular mimicry.

In molecular mimicry, foreign antigens are structurally similar to native antigens in a host, which can lead to cross reactivity in terms of the immune response. In other words, our own immune system might mistakenly recognize our own cells as foreign due to a structural resemblance between the foreign antigen and our own native proteins.

One example of molecular mimicry is how Candida albicans shares homology with tissue transglutaminase. Tissue transglutaminase is an enzyme found in the skin as well as the gut. And so this shows that Candida can actually be implicated in the path of physiology of celiac disease. Now, here’s how this could all work in an autoimmune disease.

We become infected with a microorganism which we then produce antibodies to or some T cells or both, but some of those antigens in that microorganism might also resemble some of the proteins in our own body. And as a result, our immune system mistakenly targets and attacks our body’s own cells. And over time, this can develop into an autoimmune disease if it happens enough.

So we’re gonna discuss four or five ways that tick borne disease can trigger autoimmune disease. The first, we just discussed molecular mimicry. The second is called bystander activation. The third is called epitope spreading and the fourth is called original antigenic sin. And then we’re also going to discuss a fifth just a little bit, which has to do with apoptosis or cell death.

Now, this final pathway which we’re only gonna touch on appears to be due to a TH 17 response that’s gotten a little bit out of hand and the TH 17 response in the body is associated with the autoimmune pathway. And there’s an inflammatory cytokine that’s produced by this pathway called isle 17. And when it gets a little bit out of hand, then we can end up with autoimmune disease.

But before we discuss these mechanisms that show that autoimmune disease can be triggered by a tick borne illness. Let’s talk a little bit about tick borne illness. Now, first of all, tick borne disease is transmitted by arthropods, or ticks and the tick becomes infected and it carries the infection in its blood and then that gets transmitted to its saliva.

And of course, this includes the most famous tick borne illness, Lyme disease. It also includes things like Rocky Mountain spotted fever and various co-infections such as babesia, tularemia. and plasma. Lyme disease is most famous for being prevalent in New England, particularly Connecticut. But we now know that it’s found all over the US and can even be found in various parts of the world.

We think of the classic bull’s eye rash that might appear after being bitten by an infected tick. But, we now know that probably not even the majority of people get this bull’s eye rash. Now, in my practice, probably 10 to 20% of my patients report some kind of rash that is bull’s eye like. And in the research, it’s debated, it could be anywhere from 9% to 80%.

Now, tick borne illness can also present a lot like autoimmune disease, right. We get musculoskeletal pain, Arthralgias, which are joint pain, myalgia, which is muscle pain, skin involvement, neurologic impairment, even the kidneys could be affected. And we also can see inflamed blood vessels. It’s important to note that tick borne illness or disease can lie dormant in the body for many years.

And then suddenly an infection can be triggered by something such as an illness or a trauma. And then this could down the stream trigger autoimmune disease. And we could end up with rheumatoid arthritis in our joints or hashimoto thyroiditis in our thyroid. Borrelia Burgdorferi, which is Lyme disease, is known as the great masquerader. And it can hide in different areas of our bodies in various tissues and then present as a different disease.

And many of my lime patients have various conditions and diagnoses that they’re carrying with them. And having been referred from specialist to specialist. Borrelia bacteria are shaped like a corkscrew. And I often think of them as like little Tasmanian devils. They can burrow into different organs and throw a party and wreak havoc on that particular system in the body.

They can even evade our immune system by hiding in the biofilm of the gut. So let’s discuss the first way that tick borne illness can trigger autoimmune disease in molecular mimicry. We talked about it a little bit before. One example would be in Lyme disease. A few decades ago in a study, it was discovered that what is called 41 KDA which is a protein band found in the tail of the bacteria of Borrelia also called the flagella.

Our body will make antibodies to this 41 KDA. Anyway, it was found that it shares a similar structure in human tissue with myelinated fibers in our peripheral nerves and also in the epithelial cells in our joints, particularly in the sinoval of our joints. And also there was a similarity found in heart muscle cells. And so this could, you know, just partly explain a pathogenetic role of this shared antigen in the chronic manifestations of lyme where we see joint pain, we see neuropathies, we see arthropathies and even sometimes heart involvement. A second way that tick borne illness can trigger autoimmune disease is known as the bystander effect, also called bystander activation. Basically an immune response to a pathogen takes place. And then a series of inflammatory mediators activate what are called autoreactive or self reactive T cells.

These guys are just hanging out. They just happen to be in the area and they can promote an inflammatory effect that then triggers an autoimmune disease. Bystander activation is associated with rheumatoid arthritis. Its onset or a relapse of rheumatoid arthritis also lupus and even autoimmune thyroid disease such as in hashimotos.

Basically, these self reactive cells which escaped immune tolerance will migrate to the site of inflammation and they’ll even promote more inflammation. And I think the key point here is that they’re not dependent on the antigen. A third way, the tick borne disease can trigger autoimmune disease is called epitope spreading. Epitopes are the part of an antigen that the antibody attaches to.

And when an immune response develops to a distinctly different epitope than the original disease causing one, but it has a familiar similar structure, we can get what’s called epitope spreading. From an evolutionary standpoint, this could allow our immune system to attack multiple targets like on a single pathogen if each epitope was very similar.

Now, of course, this could also lead to our own body being attacked if we had similar structures in our body that looked like that original epitope. One disease that we can see epitope spreading in is lupus where the original antibody response can be seen to spread to other regions, at least in mouse models. Now, a fourth way that tick borne disease can trigger autoimmune disease is known as original antigenic sin.

And this phenomenon occurs when there’s prior exposure to an antigen. And that prior exposure shapes subsequent or future immune responses to other related antigens such as variants. In other words, the antibody response is a little bit off target. And this is also known as immune imprinting. As we just kind of hearkened to is what we see in viral infection.

Our immune response to successive viral variants as we saw with SARS COVID two can be shaped by the original response to the exposure of the original pathogen. Now, a fifth way that tick borne disease can trigger autoimmune disease, we just kind of mentioned briefly, and this has to do with apoptosis when basically a cell is programmed to die. And there’s evidence that certain bacteria will promote self peptides, that is proteins from our own body that are then pre presented on antigen presenting cells and our own cells will then die as a result. And one example, we see this in is type 1 diabetes. We also see it in autoimmune thyroid disease and rheumatoid arthritis. Now, in type 1 diabetes, the T cells actually attack the insulin secreting beta cells in the pancreas and then they become apoptotic and die. Now, in no way is this list exhaustive.

These are just a few ways that tick borne illness could potentially trigger an autoimmune response in the body or an autoimmune disease. Finally, I’d like to talk about a couple of clinical cases I’ve seen recently where I diagnosed Bartonella and then it appeared that the bartonella triggered Hashimotos in my patients. Now, Bartonella is also known as cat scratch disease, but it’s another common tick borne co-infection transmitted in the saliva of ticks. I also found a case published about 10 years ago of an 11 year old boy who had hashimoto’s thyroiditis triggered by a bartonella infection. What’s interesting is that our thyroid, the metabolic director in our body, is like an exquisite antenna that listens to everything going on in our body, particularly for inflammation and oxidative stress.

And when there’s a lot of oxidative stress going on, it’ll begin to go a little bit haywire. And we now know that tick borne illness causes a lot of oxidative stress in individuals. And so it makes sense that Tick borne illness could indirectly lead to elevated antibodies, particularly tissue peroxidase antibodies that we see in Hashimotos.

Basically, our thyroid begins to attack itself, attacking essential enzymes that help to construct our iodine molecules which are key to building thyroglobulin and then eventually to making T3 and T4. T3 being the active form of thyroid and T4 being the inactive. And then of course, this can shut down our metabolism altogether.

The key point I want to make today is that tick borne illness should be on the differential when it comes to working with and diagnosing autoimmune disease. And because these two associated types of disease can generate a lot of oxidative stress It’s critical to take loads of antioxidants and to consume an antioxidant rich diet in order to ward off the damaging effects of these conditions. But of course, if you’re going to do that, please consult a certified or licensed holistic health care provider such as a naturopathic physician. 

That concludes today’s episode of the Modern Vital podcast. We would love to hear from you. We value your feedback. If you have any questions or suggestions, please reach out to me at ben@modernvital.com. Also, please leave us a review. If you enjoyed this episode, we look forward to having you join us next week for another exciting episode of the Modern Vital Podcast.