What the research actually shows about Borrelia, infection-driven inflammatory bowel disease, and why I have spent more than twenty years asking whether a tick changed the course of my life.

My Own Story: 2002

In 2002 I was diagnosed with Crohn's disease. I was young, I was in the thick of medical training, and I was doing everything I had been taught to do to stay well. The diagnosis arrived the way these diagnoses usually arrive: a label, a prescription, and a quiet implication that this was simply my genetic lot in life and the best I could hope for was suppression.

I never fully believed that. Not because I was stubborn, though I probably was, but because the timeline did not fit the story I was being told. My gut symptoms did not appear out of nowhere. They appeared in the wake of a febrile, relapsing, multisystem illness that I now believe was a flare of tick-borne relapsing fever caused by Borrelia miyamotoi, an organism that in 2002 was not yet even recognized as a human pathogen. The first human cases of B. miyamotoi disease were not reported until 2011 in Russia, and not until 2013 in the northeastern United States.¹ There was no test I could have asked for. There was no name for what I had.

I want to be careful here, because scientific credibility matters more to me than a satisfying narrative. I cannot prove that my Crohn's disease was caused by a relapsing fever spirochete. Nobody can prove that, in my case or anyone else's, with the tools we currently have. What I can tell you is that the biological pathway is plausible, that a growing body of published research supports the idea that infection can trigger inflammatory bowel disease in susceptible people, and that in 2023 a peer-reviewed case report described exactly this sequence in a teenage boy: Crohn's disease, an underlying Borrelia burgdorferi infection, treatment of the infection, and complete clinical remission.²

Crohn's disease is not one disease with one cause. It is a final common pathway that many different insults can lead to. The clinical question is never “is it genetic or is it environmental.” The question is: what tipped this particular person over the edge, and is any of it still active?

That question is the reason I practice functional medicine. Let me walk you through the evidence.

Crohn's Disease Is a Terrain Problem, Not a Single-Cause Problem

Inflammatory bowel disease affects millions of people worldwide, and its epidemiology has shifted dramatically since it first emerged in the Western world roughly a century ago, with the global burden now rising fastest in newly industrialized regions.³ Genes have not changed that fast. Environment has.

The modern consensus model of IBD pathogenesis involves four interlocking layers:

1. Genetic susceptibility. More than 200 IBD risk loci, many involving innate immune sensing of bacteria (NOD2, ATG16L1, IL23R).
2. A disrupted intestinal barrier. Increased permeability frequently precedes clinical disease rather than following it.
3. Microbial dysbiosis. Loss of butyrate producers, expansion of pro-inflammatory Proteobacteria.
4. An immune system that cannot switch the inflammatory response back off.

Notice what sits at the center of layers two, three, and four: microbes. And notice that the model does not require the triggering microbe to still be present when the disease becomes clinically obvious. This is a critical point, and it is where most conventional thinking about “infectious causes” goes wrong. A pathogen can light a fire and then leave the building.

The Infectious Hypothesis in IBD Is Not Fringe. It Is Old, Serious Science.

Post-infectious IBD: the population data

The cleanest evidence comes from Denmark. Gradel and colleagues followed 13,148 people with laboratory-documented Salmonella or Campylobacter gastroenteritis and 26,216 matched unexposed controls for up to 15 years. First-time IBD was diagnosed in 1.2 percent of the exposed group versus 0.5 percent of controls. The adjusted hazard ratio was 2.9 (95% CI 2.2 to 3.9). When the first year after infection was excluded, to rule out the possibility that the “gastroenteritis” was simply undiagnosed IBD, the hazard ratio was still 1.9 (95% CI 1.4 to 2.6), and the elevated risk persisted across the entire 15-year window.⁴

Read that again. A single documented bacterial gut infection roughly doubled the long-term risk of developing Crohn's disease or ulcerative colitis, and that risk was still measurable more than a decade later.

Mycobacterium avium subspecies paratuberculosis (MAP)

MAP causes Johne's disease in cattle, a chronic granulomatous enteritis that looks remarkably like Crohn's disease under the microscope. A systematic review and meta-analysis of 28 case-control studies found a pooled odds ratio of 7.01 (95% CI 3.95 to 12.4) for MAP detection by tissue PCR in Crohn's patients compared with people free of IBD.⁵ The debate over whether MAP is causal or an opportunistic passenger has run for a century and remains genuinely unresolved.⁶ A large 2026 multicenter study from a tuberculosis-endemic region again found increased association between MAP and Crohn's disease by both serology and tissue PCR.⁷

I raise MAP not because I think most Crohn's disease is mycobacterial, but to establish the principle: gastroenterology already accepts that a chronic, slow-growing, difficult-to-culture, intracellular organism can plausibly drive granulomatous bowel inflammation. Borrelia is a chronic, slow-growing, difficult-to-culture, tissue-invasive organism. The conceptual door is already open.

Where Borrelia Fits Into the Picture

The 2023 case report

In 2023, Dinetz and Saleeby published a case report in Alternative Therapies in Health and Medicine titled “Borrelia Burgdorferi, a Root Cause of Inflammatory Bowel Disease.”² A 14-year-old boy carrying an established diagnosis of Crohn's disease was found to have underlying Lyme disease. The authors treated the infection using an integrative approach, and the patient achieved complete clinical remission. On repeat serology two months into remission, B. burgdorferi p30 IgG antibodies had declined.

How much weight should this carry? This is a single patient, reported by his treating physicians, in a journal with a modest impact factor, without a control, without blinding, and without long-term follow-up published to date. It is hypothesis-generating, not practice-changing. I am telling you that plainly because you deserve to know the strength of the evidence I am handing you. What a case report can legitimately do is establish that something is possible and worth studying. This one does that.

Seroprevalence in inflammatory bowel disease

In April 2026, Aydin and Akyol published in Pathogens the first systematic look at Borrelia burgdorferi seroprevalence in an IBD population. Among 100 ulcerative colitis patients tested for B. burgdorferi IgG, 22 percent were seropositive, compared with 15.2 percent of 145 non-IBD controls drawn from the same institution and the same tick-endemic region of Türkiye.⁸

Here is where intellectual honesty is required, and where I want to be very clear with you. That difference did not reach statistical significance. And the study's other findings ran opposite to the direction you might expect: seropositive UC patients had significantly lower CRP (4.83 versus 10.50 mg/L, p = 0.020), lower uric acid, lower alkaline phosphatase, and a more stable red cell profile than seronegative patients. The authors interpret this as evidence that prior Borrelia exposure may be associated with a distinct immune-regulatory phenotype rather than active inflammatory drive, and they explicitly caution that causality cannot be established from a retrospective design with selection bias and no confirmatory two-tier testing.⁸

I could have left that paragraph out. I am including it because a blog that only reports the findings that flatter its thesis is not medicine. It is marketing. The honest summary is: Borrelia exposure is common in IBD populations from endemic areas, the relationship to disease activity is not yet characterized, and the one study we have raises as many questions as it answers.

Borrelia in gastrointestinal tissue

The gastrointestinal manifestations of tick-borne disease are documented in mainstream infectious disease literature. Zaidi and Singer reviewed GI and hepatic presentations of tick-borne illness in Clinical Infectious Diseases, concluding that abdominal signs and symptoms may provide important early diagnostic clues and urging clinicians in endemic areas to maintain a high index of suspicion.⁹

In a retrospective review of 270 patients presenting to an urban gastroenterology practice with digestive symptoms, no apparent structural pathology, and no prior diagnosis or treatment for vector-borne illness, Erdman and colleagues found a notable rate of blood-test-verified vector-borne infection.¹⁰ This is a specialty-clinic population and therefore heavily selected, but it illustrates a pattern I see constantly: the patient who has been through the full gastroenterology workup, follows a restricted diet, manages stress, and is still sick.

There is also older work from Fried and colleagues describing B. burgdorferi DNA by PCR in gastrointestinal biopsy specimens from children and adolescents with Lyme disease and chronic GI symptoms, alongside histologic gastritis, duodenitis, and colitis.¹¹ I include this because it is directly on point, and I flag it clearly: it was published in a small, non-indexed journal, the samples were tiny, and it has not been replicated in a rigorous modern study. Treat it as a signal worth investigating, not as established fact.

Six Mechanisms That Could Connect a Tick Bite to Chronic Bowel Inflammation

1. Direct tissue invasion and persistence

Borrelia burgdorferi is exquisitely tissue-tropic. It disseminates from the skin into joints, heart, nervous tissue, and connective tissue. Under stress, including antibiotic exposure, it converts into round bodies and aggregated biofilm-like microcolonies that are dramatically less susceptible to standard antibiotics. In one in vitro comparison, five antibiotics reduced biofilm-like colony formation by only 30 to 55 percent, and viable organisms remained detectable in 70 to 85 percent of biofilm colonies after treatment.¹² A detailed autopsy study documented B. burgdorferi antigens, DNA, and biofilm-form organisms in the tissues of a patient who had received extensive antibiotic therapy over a 16-year illness, with CD3+ T lymphocytes infiltrating around the biofilms.¹³

Lymphocytes clustering around a persistent bacterial biofilm is, mechanically speaking, exactly what chronic granulomatous inflammation looks like.

2. Molecular mimicry

This is the most-studied autoimmune mechanism in Lyme disease, and also the one most often oversold. Steere's group at Harvard identified that the immunodominant T-cell epitope of Borrelia outer surface protein A (OspA_165-173) shares partial sequence homology with human lymphocyte function-associated antigen 1 (hLFA-1α_L332-340), and that both peptides are presented by HLA-DR4, the allele associated with antibiotic-refractory Lyme arthritis.¹⁴

What happened next is instructive. On closer study, most OspA-reactive T-cell clones stimulated with the hLFA-1 peptide secreted IL-13, a Th2 cytokine with anti-inflammatory rather than pro-inflammatory effects, and patients with an OspA antibody response did not develop antibody reactivity to hLFA-1. In Steere's own 50-year retrospective on Lyme arthritis, he concludes that this proposed example of molecular mimicry, by itself, does not appear to explain antibiotic-refractory arthritis.¹⁵

Molecular mimicry is real, it is well described across autoimmune rheumatic disease,¹⁶ and it is almost certainly one thread in this tapestry. It is not the whole answer, and any practitioner who tells you it is has not read the follow-up literature.

3. New-onset autoimmunity after Lyme disease

This, to my mind, is the strongest and most underappreciated piece of evidence. Arvikar, Crowley, Sulka, and Steere reported a series of patients who developed new-onset systemic autoimmune joint disease, including rheumatoid arthritis, psoriatic arthritis, and peripheral spondyloarthritis, following Lyme disease.¹⁷ Note the authorship. This is not a claim from the integrative fringe. This is Steere's own group, at Massachusetts General Hospital, documenting that Lyme infection can be followed by frank, conventionally diagnosed autoimmune disease.

Crohn's disease and the spondyloarthritides share deep immunologic architecture, including HLA-B27 association, IL-23/Th17 dependence, and overlapping gut-joint inflammation. If Borrelia can precipitate peripheral spondyloarthritis, asking whether it can precipitate Crohn's disease is not a leap. It is the obvious next question.

4. Immune dysregulation and loss of resolution

Borrelia actively reshapes host immunity rather than simply provoking it. IL-10 inhibits B. burgdorferi-induced IL-17 production and attenuates IL-17-mediated Lyme arthritis.¹⁸ Infection induces the PD-1/PD-L1 checkpoint pathway, limiting T-cell infiltration into joints without compromising bacterial clearance.¹⁹ An organism that can tune checkpoint pathways and Th17 signaling is an organism capable of leaving a durable fingerprint on mucosal immune regulation long after it is gone.

5. Barrier disruption and dysbiosis

Morrissette and colleagues, working with the Johns Hopkins SLICE cohort, found that 87 rigorously characterized patients with post-treatment Lyme disease syndrome had a gut microbiome signature distinct from both healthy controls and ICU patients, with over 80 percent classification accuracy. The signature involved increased Blautia, decreased Bacteroides, and, in roughly one in five patients, a relative abundance of pro-inflammatory Enterobacteriaceae above 10 percent. Critically, the pattern did not cluster by antibiotic history, meaning antibiotic exposure alone did not explain it.²⁰

Depleted Bacteroides means fewer short-chain fatty acids, less butyrate, weaker regulatory T-cell induction, and a less well-fed colonocyte. Expanded Enterobacteriaceae means more lipopolysaccharide at the barrier. That is the biochemical recipe for a leaky, inflamed gut. If you want the deeper dive on this pathway, I have written about it at length in Zonulin: The Master Gatekeeper of Your Gut and in Leaky Gut Syndrome: Could a Complex Protein Named Zonulin Be to Blame?

6. Co-infections and cumulative burden

A single tick can carry multiple organisms. Babesia, Bartonella, Anaplasma, Ehrlichia, and relapsing fever Borrelia each bring their own immunologic signature, and the combination is rarely the sum of its parts. I have covered this terrain in Tick-Borne Illnesses and the Gut and in The Hidden Epidemic: Understanding Chronic Lyme Disease.

Why Borrelia miyamotoi Deserves Its Own Section

Most conversations about tick-borne disease stop at B. burgdorferi. That is a mistake, and it is a personal one for me.

Borrelia miyamotoi is carried by the same Ixodes ticks that transmit Lyme disease, yet it is genetically and ecologically distinct, grouping instead with the relapsing fever Borrelia. For this reason it has been given its own designation: hard tick relapsing fever.^1,21 Four things about it matter enormously for anyone thinking about gut disease.

Seroprevalence in endemic areas of the northeastern United States has been estimated at roughly 2.8 percent, compared with about 11 percent for prior Lyme disease.²² That is not rare. That is roughly one in thirty-five people in tick-endemic regions with serologic evidence of exposure to an organism that most physicians have never tested for.

An important gap. To my knowledge there is no published study specifically linking Borrelia miyamotoi to inflammatory bowel disease. My own belief about my 2002 diagnosis rests on biological plausibility, clinical timeline, and the documented GI involvement of hard tick relapsing fever. It does not rest on direct evidence, and I will not pretend otherwise. I share it because patients tell me all the time that their illness “started after something,” and I want them to know that a physician takes that observation seriously.

If you want a fuller primer on this family of organisms, see Tick-Borne Relapsing Fever: What You Need to Know.

What This Means in the Exam Room

When I consider tick-borne infection in someone with IBD

I am not suggesting that every person with Crohn's disease has Lyme disease. Most do not. But I raise the question when several of the following cluster together:

• Onset of GI disease in the weeks to months following a febrile, flu-like, or multisystem illness, particularly one occurring in late spring or summer
• Known tick exposure, outdoor occupation or recreation, or residence in an endemic region
• Prominent extraintestinal features that are out of proportion to the bowel disease: migratory arthralgias, neuropathic pain, air hunger, night sweats, temperature dysregulation, cognitive fog, or new dysautonomia
• Inadequate or unusually short-lived response to appropriately dosed conventional IBD therapy
• Relapsing, cyclical symptom patterns rather than the steadier course typical of uncomplicated IBD
• Coexisting mast cell activation features, which frequently accompany chronic infection

Testing considerations

Standard two-tier Lyme testing misses a substantial share of early cases and, as noted above, will not detect relapsing fever Borrelia at all. If the clinical picture warrants it, I consider adding B. miyamotoi-specific testing (PCR in acute febrile illness, GlpQ serology thereafter), co-infection panels, and inflammatory and immune markers rather than relying on a single negative ELISA to close the question.

What I do not do

I do not take people off appropriate conventional therapy in order to chase an infectious hypothesis. If you are in remission on a biologic, that remission is real and it is protecting your bowel from irreversible structural damage. Stricturing, fistulizing, and dysplastic complications of untreated Crohn's disease are not theoretical. Investigating a possible infectious contributor and continuing your gastroenterologist's treatment plan are not mutually exclusive, and any practitioner who frames them as an either-or is putting ideology ahead of your intestine.

Root cause medicine is additive, not subtractive. We add the missing question. We do not subtract the treatment that is keeping you out of the operating room.

Supporting the Terrain While You Investigate

Whether or not a tick-borne organism turns out to be part of your story, the downstream biology is worth addressing directly: barrier integrity, microbial balance, immune tone, and the inflammatory environment of the gut. These are the products I most often reach for in my own practice, and I have written about the broader framework in How to Heal Your Gut for a Stronger Immune System.

Barrier and mucosal support

• Dr. Jill Health® Gut Shield, providing 4 g of L-glutamine along with DGL licorice and supporting nutrients for GI barrier integrity
• Dr. Jill Health® Gut Immune, featuring ImmunoLin® serum-derived immunoglobulin G, which binds microbial antigens and toxins within the GI lumen
• Sodium Butyrate, delivering the short-chain fatty acid most depleted when Bacteroides populations fall

Microbiome restoration

• Ther-Biotic Complete for broad-spectrum multi-strain support
• Dr. Jill Health® Probiotic 100 Billion Plus when higher-dose support is warranted, particularly during or after antimicrobial therapy

Biofilm and circulatory support

• LumbroPro and BloodFlowPro, which provide fibrinolytic enzymes including lumbrokinase and nattokinase to help degrade the fibrin matrix that stabilizes bacterial biofilms

Botanical antimicrobial support, under clinical supervision

• Cryptolepis and Samento (cat's claw), among the botanicals that showed the strongest activity against stationary-phase Borrelia in Johns Hopkins laboratory screening
• NUTRA-BRL for comprehensive microbial and immune support in Lyme and tick-borne relapsing fever, and NUTRA-BBS or NUTRA-BRT when co-infections are part of the picture

You can browse the full Dr. Jill Health Gut Support collection for the complete range. Please work with a clinician who knows your case before beginning any antimicrobial protocol, especially if you have active bowel inflammation. Herxheimer reactions in an already inflamed intestine are not trivial, and dosing needs to be gentle, slow, and supervised.

What We Still Do Not Know

I want to close the scientific section by naming the gaps clearly, because you will not find this list in most articles on the topic:

• We have no controlled trial of antimicrobial therapy for IBD patients with documented Borrelia exposure. Not one.
• We have no prospective cohort measuring IBD incidence after confirmed Lyme disease, the way Gradel measured it after Salmonella.
• The single seroprevalence study we have found lower, not higher, inflammatory markers in seropositive UC patients, a finding that no current model comfortably explains.⁸
• Molecular mimicry between OspA and hLFA-1, once the leading mechanistic explanation, has not held up as a sufficient explanation even for Lyme arthritis.¹⁵
• Detection of bacterial DNA in inflamed tissue does not establish causation. It may reflect a permeable, inflamed barrier admitting passengers.

Uncertainty is not a reason to dismiss the hypothesis. It is a reason to fund the studies. And in the meantime, it is a reason for clinicians to ask better questions of the patient in front of them.

A word about the part of healing that no journal indexes.

I spent years angry at my own body. I understand the particular loneliness of a diagnosis that arrives with a shrug, and the exhaustion of being the only person in the room who still believes there is an answer. If that is where you are sitting right now, I want you to hear this: your observation about when your illness started is data. Your body is not lying to you. And you are allowed to keep asking.

What carried me through was not only the science, though the science mattered enormously. It was prayer, and the stubborn conviction that I was held even in the years when nothing made sense and no test came back useful. I have watched that same quiet, unmeasurable thing change the trajectory of patients whose labs said they should not have recovered. I cannot put a p-value on it. I have stopped trying. I simply tell people the truth: bring your whole self to this, the biochemistry and the spirit both, and do not let anyone convince you that hope is unscientific.

I wrote about all of it in Unexpected: Finding Resilience Through Functional Medicine, Science, and Faith, including the parts I was afraid to say out loud.

Where to Go From Here

If you have inflammatory bowel disease and something about your story has never added up, bring this article to your next appointment. Ask about the timeline. Ask whether tick-borne infection was ever considered and, if serology was done, whether it was capable of detecting relapsing fever Borrelia at all. Ask what else could be driving the fire.

At Flatiron Functional Medicine in Louisville, Colorado, we work with complex chronic illness every day, including tick-borne disease, mold and mycotoxin illness, mast cell activation, and autoimmune bowel disease. You can learn more at jillcarnahan.com.

Twenty-four years after my own diagnosis, I am well. Not because someone handed me a single answer, but because a series of people were willing to keep asking questions after the obvious ones ran out. I would like to be that person for you.

References

1. Wagemakers A, Staarink PJ, Sprong H, Hovius JW. Borrelia miyamotoi: a widespread tick-borne relapsing fever spirochete. Trends Parasitol. 2015;31(6):260-269. doi:10.1016/j.pt.2015.03.008
2. Dinetz E, Saleeby Y. Borrelia Burgdorferi, a Root Cause of Inflammatory Bowel Disease: A Case Report of Successful Treatment and Remission. Altern Ther Health Med. 2023;29(5):86-89. PMID: 37392196
3. Agrawal M, Jess T. Implications of the changing epidemiology of inflammatory bowel disease in a changing world. United European Gastroenterol J. 2022;10(10):1113-1120. doi:10.1002/ueg2.12317
4. Gradel KO, Nielsen HL, Schønheyder HC, Ejlertsen T, Kristensen B, Nielsen H. Increased short- and long-term risk of inflammatory bowel disease after Salmonella or Campylobacter gastroenteritis. Gastroenterology. 2009;137(2):495-501. doi:10.1053/j.gastro.2009.04.001
5. Feller M, Huwiler K, Stephan R, et al. Mycobacterium avium subspecies paratuberculosis and Crohn's disease: a systematic review and meta-analysis. Lancet Infect Dis. 2007;7(9):607-613. doi:10.1016/S1473-3099(07)70211-6
6. Mintz MJ, Lukin DJ. Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn's disease: the debate continues. Transl Gastroenterol Hepatol. 2023;8:28. doi:10.21037/tgh-23-16
7. Vuyyuru SK, Singh U, Das P, et al. Association of Mycobacterium avium paratuberculosis With Crohn's Disease: A Large Multicenter Study From a Tuberculosis-Endemic Region. Clin Infect Dis. 2026;82(5):841-847. doi:10.1093/cid/ciaf738
8. Aydin G, Akyol T. Seroprevalence of Borrelia burgdorferi Antibodies in Patients with Ulcerative Colitis and Its Association with Disease Activity. Pathogens. 2026;15(4):408. doi:10.3390/pathogens15040408
9. Zaidi SA, Singer C. Gastrointestinal and hepatic manifestations of tickborne diseases in the United States. Clin Infect Dis. 2002;34(9):1206-1212. doi:10.1086/339871
10. Erdman MD, Kossari N, Ye J, Reynolds KH, Blodget E, Mozayeni BR, Rahbar FS. Association of Presenting Symptoms With Abnormal Laboratory Values for Vector-Borne Illness: Experience in an Urban Gastroenterology Practice. J Patient Cent Res Rev. 2021;8(1):39-47. doi:10.17294/2330-0698.1729
11. Fried MD, Pietrucha D, Madigan G, Bal A. Borrelia burgdorferi persists in the gastrointestinal tract of children and adolescents with Lyme disease. J Spirochetal Tick-borne Dis. 2002;9(1):11-15. (Small case series in a non-indexed journal; low evidence tier, cited here as a historical signal only.)
12. Sapi E, Kaur N, Anyanwu S, et al. Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi. Infect Drug Resist. 2011;4:97-113. PMID: 21753890
13. Sapi E, Kasliwala RS, Ismail H, et al. The Long-Term Persistence of Borrelia burgdorferi Antigens and DNA in the Tissues of a Patient with Lyme Disease. Antibiotics (Basel). 2019;8(4):183. doi:10.3390/antibiotics8040183
14. Trollmo C, Meyer AL, Steere AC, Hafler DA, Huber BT. Molecular mimicry in Lyme arthritis demonstrated at the single cell level: LFA-1 alpha L is a partial agonist for outer surface protein A-reactive T cells. J Immunol. 2001;166(8):5286-5291. PMID: 11290815
15. Steere AC. Lyme Arthritis: A 50-Year Journey. J Infect Dis. 2024;230(Suppl 1):S1-S10. doi:10.1093/infdis/jiae126
16. Fehringer M, Vogl T. Molecular mimicry in the pathogenesis of autoimmune rheumatic diseases. J Transl Autoimmun. 2025;10:100269. doi:10.1016/j.jtauto.2025.100269
17. Arvikar SL, Crowley JT, Sulka KB, Steere AC. Autoimmune arthritides, rheumatoid arthritis, psoriatic arthritis, or peripheral spondyloarthritis following Lyme disease. Arthritis Rheumatol. 2017;69(1):194-202. doi:10.1002/art.39866
18. Hansen ES, Medić V, Kuo J, Warner TF, Schell RF, Nardelli DT. Interleukin-10 (IL-10) inhibits Borrelia burgdorferi-induced IL-17 production and attenuates IL-17-mediated Lyme arthritis. Infect Immun. 2013;81(12):4421-4430. doi:10.1128/iai.01129-13
19. Helble JD, McCarthy JE, Sawden M, Starnbach MN, Hu LT. The PD-1/PD-L1 pathway is induced during Borrelia burgdorferi infection and inhibits T cell joint infiltration without compromising bacterial clearance. PLoS Pathog. 2022;18(10):e1010903. doi:10.1371/journal.ppat.1010903
20. Morrissette M, Pitt N, González A, et al. A Distinct Microbiome Signature in Posttreatment Lyme Disease Patients. mBio. 2020;11(5):e02310-20. doi:10.1128/mbio.02310-20
21. Cleveland DW, Anderson CC, Brissette CA. Borrelia miyamotoi: A Comprehensive Review. Pathogens. 2023;12(2):267. doi:10.3390/pathogens12020267
22. McCormick DW, Brown CM, Bjork J, et al. Characteristics of Hard Tick Relapsing Fever Caused by Borrelia miyamotoi, United States, 2013-2019. Emerg Infect Dis. 2023;29(9). Full text

Every reference above was independently verified against the publisher of record or PubMed at the time of writing, and every DOI and link was confirmed to resolve. Reference 11 is retained deliberately despite its low evidence tier and is labeled as such in the list rather than presented alongside peer-reviewed indexed work without comment.

Dr. Jill C. Carnahan, MD, ABIHM, ABoIM, IFMCP is a triple board-certified functional medicine physician and Medical Director of Flatiron Functional Medicine in Louisville, Colorado. She is the author of the bestselling book Unexpected: Finding Resilience Through Functional Medicine, Science, and Faith, host of the Resiliency Radio podcast, and is featured in the Doctor/Patient documentary. Follow her at jillcarnahan.com and @drjillcarnahan on Instagram.

These statements have not been evaluated by the Food and Drug Administration. The products mentioned in this article are not intended to diagnose, treat, cure, or prevent any disease. The information in this article is not intended to replace any recommendations from or relationship with your physician, and it is not medical advice. Do not discontinue prescribed therapy for inflammatory bowel disease without consulting your treating gastroenterologist. Please review the references cited at the end of the article for scientific support of any claims made.