Archive for the ‘Lyme’ Category

Virtual Hackathon: Educate & Elevate For Tick-Borne Illness Team Pitches & Awards


Virtual Hackathon: Educate & Elevate For Tick-Borne Illness Team Pitches & Awards

Innovative teams are competing for grant funding to shift existing paradigms in Tick-Borne Illness.

The goal of this virtual program is to create projects that educate the public and institutions that hold the keys to meaningful change. By taking on this challenge, they will contribute to easing senseless suffering that is caused by a simple tick bite.

Speakers, entertainment, and a chance to make a difference.

When: Saturday October 24, 2020

Time: 1pm ET

Register to receive the Zoom link:

Senator Collins Announces $25 Million Initiative to Fight Lyme Disease’-announces-25-million-initiative-fight-lyme-disease

Senator Collins Announces $25 Million Initiative to Fight Lyme Disease

Last year, Senator Collins authored a new law that provides $150 million over five years to fight tick-borne illnesses.

Washington, D.C.— U.S. Senator Susan Collins, a member of the Health Committee, announced the launch of LymeX, a new $25 million effort to fight tick-borne diseases.  LymeX is the largest public-private partnership to combat Lyme disease in history and will provide awards to improve data about tick-borne diseases; raise awareness; and accelerate the discovery of diagnostic tools, testing, and implementation.  Senator Collins, the author of the Kay Hagan Tick Act that became law last year, received a call today from Department of Health and Human Services (HHS) Deputy Secretary Eric Hargan, who shared this positive development.

LymeX is being led by HHS and the Steven & Alexandra Cohen Foundation and will be housed within the HHS Office of the Assistant Secretary for Health, the coordinating agency developing the National Strategy to fight tick-borne diseases that was required by Senator Collins’ Tick Act.  LymeX augments the Tick Act law and reinforces the federal focus on this priority.

“This partnership is an exciting and promising development in our fight against tick-borne illnesses such as Lyme disease that affect hundreds of thousands of Americans every year.  As the largest public-private partnership to combat Lyme disease in history, this initiative builds on the bipartisan TICK Act I authored and demonstrates that the federal government is focused on eradicating this public health threat,” said Senator Collins.  “I remain committed to slowing the spread of these devastating diseases, and I will continue my efforts to protect Mainers’ health.”

Specifically, LymeX will advance tick-borne disease innovation by incentivizing the development of next-generation diagnostics through a series of multi-million-dollar grand prize challenges. The first LymeX diagnostics prize will launch in 2021. These prizes will be open to U.S. universities, non-profit organizations, private-sector companies, and domestic organizations to improve diagnostics at all stages of Lyme disease.

The initiative will also engage stakeholders to facilitate patient-centered innovations to address tick-borne diseases and increase education to raise awareness about risk and prevention.

The incidence of Lyme and other tick-borne diseases has exploded over the past 15 years.  In 2003, Lyme disease infected around 30,000 Americans.  The latest estimates show there are nearly half a million Americans suffering from Lyme.  In Maine, there were a record 2,167 newly reported cases of Lyme disease last year, nearly triple the number of cases in 2010.  Other tick-borne diseases are also on the rise – in Maine, for example, Anaplasmosis and Babesiosis have increased several-fold in this same period.

LymeX will complement the three-pronged approach created by Senator Collins’ Tick Act law, which:

  1. Requires HHS to develop a National Strategy.  This will help expand research, improve testing and treatment, and coordinate common efforts across federal agencies including with DOD, USDA, EPA, the VA, and the Departments of Interior and Homeland Security
  2. Reauthorizes Regional Centers of Excellence in Vector-Borne Disease for five years at $10 million per year.  These Centers have led the scientific response against tick-borne diseases, which now make up 75 percent of vector-borne diseases in the U.S.
  3. Authorizes CDC Grants at $20 million per year for State Health Departments to improve data collection and analysis, support early detection and diagnosis, improve treatment, and raise awareness.  These awards will help states build a public health infrastructure for Lyme and other tick and vector-borne diseases and amplify their initiatives through public-private partnerships.



Involving the HHS will almost certainly doom this project.  We should learn from history.  The anti-patient bias is clear and has remained unchanged:


Remarks made after the vote made it clear that the abstainers felt they had defeated the measure, because “yes” votes didn’t comprise a majority of panel members. But, oops, guess what? Abstentions don’t count one way or the other. So, the recommendation passed, 5-3.

As that reality sank in, pandemonium broke out. Panelist Scott Commins stoutly announced that he wanted to change his abstaining vote to “no.” He was told that Robert’s Rules of Order don’t allow you to change your vote after the fact.

Things then got very bizarre very fast, with many people talking at once. Some wanted to vote on the original question again. Others didn’t. Some wanted to re-open discussion, others didn’t. It was confusing to the listener at home.

However, the five abstainers sure gave the impression they had been trying to game the system—to gain a “no” vote without having to publicly own up to it. When that ploy didn’t work, they scrambled to recoup their original objective— to deep-six the proposal regarding persistent Lyme disease.

It is truly time for a CDC/NIH/IDSA/HHS walkout movement. Our public health ‘authorities’ have vested interests which interfere with doing what is right for patients. We’ve tried working with them for over 40 years.  How many times are you going to get behind a horse that kicks you?  Although Weiler is discussing how ‘authorities’ have handled COVID, the exact same things could be said about how they’ve handled Lyme/MSIDS. 

Public ‘authorities’ should not be allowed to own patents on things that interfere with their ability to make public health decisions.

For more: ConflictReport

More Evidence of Lyme Organism Persistence. Peptidoglycan is only Produced by Metabolically-Active Spirochetes.


Front. Cell. Infect. Microbiol., 07 October 2020 |

Mechanisms of Dysregulated Antibody Response in Lyme Disease

  • 1Global Lyme Alliance, Inc., Stamford, CT, United States
  • 2Edge Bioscience Communications, Sherborn, MA, United States


Lyme disease (LD), caused by the spirochetal bacterium Borrelia burgdorferi, is transmitted by the black-legged tick Ixodes scapularis (Hu, 2016). LD is the fastest growing global tick-borne disease and annually affects >300,000 people in the U.S. alone (Steere et al., 2016). The economic impact is a staggering $1.3 billion dollars per year (Adrion et al., 2015). LD can cause long-term, debilitating symptoms, including arthritis, carditis, and neurological complications (Hu, 2016; Steere et al., 2016). A longstanding question is why antibodies produced during primary infection are not able to completely clear spirochetes or confer protective immunity (Barbour et al., 2008). Antibody titers can remain for years in some LD patients while in others, they wane over time or never develop at all (Kalish et al., 2001). Herein, we describe animal studies that reveal mechanisms behind dysregulated development of adaptive immunity and provide insights that may be relevant to human immunity to B. burgdorferi infection.

Role of Lymphocytes and Antibodies in Lyme Disease Pathogenesis

Antibodies produced through B and T cell interactions either within or outside germinal centers are termed T cell-dependent (TD) whereas those produced without the aid of T cells are T cell-independent (TI). One mechanism whereby B. burgdorferi attempt to evade adaptive immunity is by continuously changing the sequence of a unique surface protein called variable major protein-like sequence (VlsE) (Norris, 2015). Such sequence variation generates a large repertoire of antigenically-distinct spirochetes that become unrecognizable to the antibodies that are mounted against a previous version of this protein. This may allow B. burgdorferi to persist for months or years if not effectively cleared through innate immune response and/or early diagnosis and treatment with antibiotics. Another defensive strategy relies on switching which immunogenic proteins are surface expressed [e.g., Outer Surface Protein A (OspA) and OspC], as spirochetes transit from one environment to another. OspA and OspC are predominately expressed when spirochetes are in the tick vs. the mammalian host, respectively. Notably, whole-proteome microarray analysis revealed that while relatively few B. burgdorferi open reading frames (~15%) encode immunogens, those that do elicit the same detectable antibodies in naturally infected humans and wild white-footed mice (Peromyscus leucopus), the predominant maintenance reservoir for B. burgdorferi (Barbour et al., 2008). Interestingly, a spectrum of disease severity has been observed in different mouse strains, reflecting their unique genetic composition, which controls the magnitude of humoral responses during B. burgdorferi infection (Weis et al., 1999).

Despite strong antibody responses in animals experimentally-infected with B. burgdorferi and in many LD patients, this does not translate to robust disease-resolving and long-term immunity (Barthold and Bockenstedt, 1993; Aguero-Rosenfeld et al., 1996). In order to explore the mechanisms through which B. burgdorferi infection impacts the immune system and gain an understanding of the role of B and T cells in LD pathogenesis, researchers have conducted studies in mice lacking either or both of these lymphocyte populations.

Pathologies associated with B. burgdorferi infection of mice often spontaneously resolve, although animals may never completely clear spirochetes. In contrast, after infection with B. burgdorferi, severe combined immunodeficient (SCID) and recombination activating gene (RAG)-deficient mice, both of which lack B and T cells, developed severe, persistent arthritis that remained unresolved (Hastey et al., 2012). While B cells regulate disease progression and resolution in wild-type mice (McKisic and Barthold, 2000), adoptive transfer of CD4+ T cells into RAG-deficient mice prior to B. burgdorferi infection increased arthritis and carditis severity (unless B cells were co-transferred), and CD8+ T cell transfer increased arthritis severity (McKisic et al., 2000). Conversely, adoptive transfer of serum from immunocompetent B. burgdorferi-infected mice into SCID mice ameliorated both arthritis and carditis (Barthold et al., 1997; McKisic and Barthold, 2000). Transfer of immune serum into naive recipient mice either prior to or at the time of inoculation also prevented B. burgdorferi infection (Barthold et al., 1997). Immunization of mice with late-stage LD patient sera that demonstrated strong antibody reactivity to several B. burgdorferi proteins, including OspA and B, provided partial protection against B. burgdorferi challenge (Fikrig et al., 1994). These findings reveal that humoral immune responses generated in experimentally-infected mice and LD patients play an important role in the resolution of some of the most commonly reported clinical manifestations (arthritis and carditis), which are driven principally by activation of inflammatory T cells and release of potent inflammatory mediators.

Researchers found unusually strong and persistent TD and TI IgM antibody production in lymph nodes during early infection and in bone marrow later on in the course of murine infection (Hastey et al., 2012; Richards et al., 2015). IgG-secreting plasma cells, on the other hand, accumulate slowly in the bone marrow. Only about 50% of the IgG response is clearly TD and, coupled with IgM, is thought to contribute to the reduction but not elimination of B. burgdorferi from tissues (Hodzic et al., 2003). This TD repertoire of IgG contributes minimally to long-term antibody-mediated immunity, unlike the typical humoral response to bacterial pathogens (Hastey et al., 2012; Tracy and Baumgarth, 2017).

Mechanism(s) of Immune Dysfunction in Lyme Disease

To dissect the mechanisms behind this dysregulated response, Hastey et al. (2012) elucidated distinct stages of altered immune response using a mouse model of LD. In the first phase of infection, B cells accumulated in lymph nodes and induced antibodies in a TI manner and in the absence of germinal centers. In other infectious diseases, such as mumps and HIV, swollen lymph nodes are a frequent early symptom of infection. Normally, the areas in which T and B cells are found in lymph nodes are well-defined. However, in B. burgdorferi-infected mice, this typical architecture was disrupted, with loss of organized B cell follicles and T cell zones (Tunev et al., 2011). Deterioration of B cell follicles, between days 5 and 10 post-infection occurred together with the presence of spirochetes within the lymph nodes (Hastey et al., 2014). In addition, B cells began to accumulate in large numbers, reaching over 70% in some instances and disrupting normal T/B cell ratios (Hastey et al., 2012).

In the second phase, roughly 2–3 weeks later, short-lived germinal centers developed in lymph nodes. These germinal centers gave rise to relatively few antibody-producing plasma cells within bone marrow, leading to a third phase in which plasma cells only slowly accumulated. Lymph node germinal centers disappeared about 1 month after infection, despite the continued presence of bacteria at these sites. Curiously, B cell accumulation occurred after, not before, destructive changes in lymph node morphology. This suggests that the Borrelia infection, not B cell accumulation, somehow drives lymphoid tissue atrophy (Hastey et al., 2014).

So, while B. burgdorferi infection prompts strong serum antibody levels, and titers increase over the course of infection, the antibody response is ultimately ineffective in completely eradicating spirochetes and/or establishing long-term immunity (Tunev et al., 2011; Hastey et al., 2012; Elsner et al., 2015). B. burgdorferi benefits from this maladaptive immune response. This premise is corroborated by a study of antibiotic-treated human LD patients, which included patients who had persistent symptomatology and those who had returned to health within 6 months after diagnosis and treatment (Blum et al., 2018). The researchers focused on plasmablasts, activated B cells that mature into plasma cells within germinal centers. They found that patients who ultimately recovered their health, as compared to those with persistent symptoms, had significantly more plasmablasts during early infection. The researchers determined this by comparing the percentage of plasmablasts as a total of all B cells at the initial clinic visit, during early infection (even before beginning Doxycycline therapy). In addition, patients who ultimately returned to health had significantly higher titers of antibodies to a diverse array of B. burgdorferi proteins (Blum et al., 2018). Taken together, this is evidence that B. burgdorferi infection redirects the adaptive immune system away from a long-term protective antibody response and toward a less efficacious, rapid and strong, though short-lived antibody response (Richards et al., 2015).

Interestingly, Hastey et al. (2014) also provided evidence that Borrelia infection itself may have broader immunosuppressive effects. They tested this by using influenza virus vaccination as a tool to study TD antibody responses. Two groups of mice were influenza-vaccinated, with one group being infected with B. burgdorferi while the other was not. For the first 3 weeks, both groups of mice produced similar amounts of influenza-specific IgG. However, by 4 weeks, and until the study ended at 26 weeks, the B. burgdorferi-infected animals made significantly less influenza-specific IgG than the uninfected mice. By 9 weeks post-infection, there were far fewer influenza-specific antibody-secreting cells in the bone marrow of the Borrelia-infected animals compared to uninfected influenza-vaccinated mice (Elsner et al., 2015). This finding engenders an intriguing question about whether LD might negatively impact vaccination efficacy.

Implications for Diagnostics

There is more to be done in exploring these mechanisms of dysregulated antibody response in LD patients and there are clear implications for development of improved diagnostic tests. Physicians often follow the CDC-recommended two-tiered testing algorithm to detect B. burgdorferi-specific antibodies in patients suspected of having LD (Marques, 2015). The first-tier test is an enzyme-linked immunosorbent assay or ELISA, and if results are positive or borderline, a confirmatory second-tier test is done; a Western immunoblot analysis to detect IgM and IgG antibodies that are specific for B. burgdorferi proteins. In theory, this test determines if a B. burgdorferi infection is active (Marques, 2015). However, this CDC-recommended serodiagnosis may be misleading. In a small study of 79 patients who no longer had symptoms, but had a history of LD with and without arthritis 10–20 years ago, researchers examined antibody titers using the CDC two-tiered test (Kalish et al., 2001). They found that 10 individuals (13%) currently had IgM responses (reflecting initial exposure) to B. burgdorferi and 34 (43%) had IgG reactivity (reflecting longer term exposure) to B. burgdorferi. Antibody titers were even higher for patients who had LD with arthritis (but were currently asymptomatic), as six of 39 (15%) currently had IgM responses and 24 of 39 (62%) had IgG reactivity. This trend also is seen in infected mice, where IgM antibody levels do not wane but stay relatively high along with the increased IgG response (Hastey et al., 2012).

Theoretically, it would be expected that all recovered patients would lack evidence of IgM and many or all would continue to have circulating IgG. The presence of IgM in 13% of patients would be cause for confusion for physicians as the presence of this class of antibody typically wanes with clearance of the pathogen and recovery from infection. Larger studies need to be done to confirm and to explain the reasons for the continued presence of IgM. Another consideration is that high antibody levels, as discussed, may only offer transient protection, with alterations in germinal center architecture and defective production of long-lived plasma cells and memory cells leading to poor immunoprotection in the long-term (Hastey et al., 2012; Elsner et al., 2015).

Future efforts in Lyme disease diagnosis need to focus on distinguishing between active and inactive infection and improving sensitivity in detecting early disease while maintaining high specificity. Diagnosis would be greatly enhanced with the development and broad adoption of point-of-care testing, and simplified diagnosis. Addition of antigen targets expressed very early in LD (e.g., VlsE1 and pepC10) to current antibody-based diagnostic testing procedures have enhanced performance of the diagnostic assays (Porwancher et al., 2011; Marques, 2015). Additionally, direct detection of B. burgdorferi antigens or nucleic acid rather than antibody testing may eventually be possible with the development of advanced technologies (Branda et al., 2018). Not only might direct detection of spirochetal components be indicative of active infection, but the presence of nucleic acids and certain antigens coincides with the earliest stage of infection, when B. burgdorferi-specific antibodies have yet to be produced. Examples include B. burgdorferi DNA detected using PCR (Mosel et al., 2019) and antigens such as OspC (Ohnishi et al., 2001) or peptidoglycan (Jutras et al., 2019). OspC is expressed on spirochetes as they transit from tick to mammalian host (Ohnishi et al., 2001) while peptidoglycan has been shown to persist in patients long after antibiotic treatment has ceased and patients are theoretically cured of active infection (Jutras et al., 2019).

The latter observation strongly supports the notion of persistence of B. burgdorferi after antibiotic treatment as peptidoglycan is only produced by metabolically-active spirochetes.


There has been significant progress in deciphering the mechanistic foundation of B. burgdorferi’s impact on the adaptive immune response, specifically the B cell response and antibody production. While B. burgdorferi initially elicits a strong immune response, the end result is a failure by the immune system to clear the infection. This could set the stage for B. burgdorferi’s persistence (Tracy and Baumgarth, 2017), which may underlie chronic symptoms such as arthritis, carditis, and skin and neurological complications. The many animal studies conducted to date reveal that B. burgdorferi relies upon multiple strategies to evade and disrupt the normal functioning of the immune system. The end results are inhibition of effective B cell responses, disruption of the formation of stable germinal centers, and dampening the production of optimally protective antibodies and establishment of long-term memory cell populations. Importantly, many of these same evasion strategies appear to be employed by B. burgdorferi in LD patients, particularly those suffering from persistent or chronic disease. These intriguing observations provide an excellent foundation and springboard for further animal and human studies, with the goal of increased understanding of LD pathogenesis, better diagnostics, and ultimately novel and more effective therapeutic options for long-suffering patients.

Author Contributions

DB and TS contributed to the writing of this manuscript. All authors contributed to the article and approved the submitted version.

Funding: Publication of this manuscript was financially supported by Global Lyme Alliance, Inc.

Conflict of Interest

DB is the owner of Edge Bioscience Communications, a freelance, contract scientific/medical writing and consulting company.

The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


We would like to acknowledge Drs. Mayla Hsu and Nicole Baumgarth for thoughtful review of this manuscript prior to its submission for review.


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Citation: Sellati TJ and Barberio DM (2020) Mechanisms of Dysregulated Antibody Response in Lyme Disease. Front. Cell. Infect. Microbiol. 10:567252. doi: 10.3389/fcimb.2020.567252

Received: 29 May 2020; Accepted: 02 September 2020;
Published: 07 October 2020.

Edited by:  John M. Leong, Tufts University School of Medicine, United States

Reviewed by:  Rachel Maurie Gerstein, University of Massachusetts Medical School, United States, Ronald Mark Wooten, University of Toledo, United States

Copyright © 2020 Sellati and Barberio. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Timothy J. Sellati,


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FREE Webinar on Vibrant’s New Expanded Tickborne & Infections Panels


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Join Vibrant and Amy Offutt MD for an introduction and discussion of Vibrant’s new expanded tickborne and infections panels, including additional Lyme and TBRF markers, added coinfections, and now with opportunistic infections commonly missed alongside Lyme and coinfections.
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Dr. Amy Offutt is a director on the ILADS board, and the medical director and co-owner of Heart & Soul Integrative Health and Yoga located in Marble Falls, Texas. She completed her undergraduate studies at Abilene Christian University, medical school at The University of Texas Health Sciences Center in San Antonio, and a residency in Family Medicine at Christus Health. She also has a Master’s Degree in Integrative Medicine from George Washington University and has completed a fellowship in Integrative Medicine. Her calling to look for the cause of disease, in addition to how to manage symptoms, led to her appointment by Governor Greg Abbott to the Pediatric Acute-Onset Neuropsychiatric Syndrome Advisory Council in the summer of 2019. She has been married to her high school sweetheart, Brad, for 30 years, and they have 3 children, ages 19, 17, and 12. They enjoy family time, being on the lake, traveling, and healthy living.

Chest Palpitations in a Teenager as Unusual Presentation of Lyme Disease: Case Report

Chest palpitations in a teenager as an unusual presentation of Lyme disease: case report

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Background: The incidence of Lyme disease (LD) in North America has increased substantially in the past two decades. Concomitant with the increased incidence of infection has been an enhancement in the recognition of LD complications. Here, we report a case of Lyme carditis complicated by heart block in a pediatric patient admitted to our children’s hospital. What is unique about this case is that the complaint of chest palpitations is an infrequent presentation of LD, and what it adds to the scientific literature is an improved understanding of LD in the pediatric population.

Case presentation: The patient was a 16-year-old male who presented with the main concerns of acute onset of palpitations and chest pain. An important clinical finding was Erythema migrans (EM) on physical exam. The primary diagnoses were LD with associated Lyme carditis, based on the finding of 1st degree atrioventricular heart block (AVB) and positive IgM and IgG antibodies to Borrelia burgdorferi. Interventions included echocardiography, electrocardiography (EKG), and intravenous antibiotics. The hospital course was further remarkable for transition to 2nd degree heart block and transient episodes of complete heart block. A normal sinus rhythm and PR interval were restored after antibiotic therapy and the primary outcome was that of an uneventful recovery.

Conclusions: Lyme carditis occurs in < 5% of LD cases, but the “take-away” lesson of this case is that carditis can be the presenting manifestation of B. burgdorferi infection in pediatric patients. Any patient with suspected Lyme carditis manifesting cardiac symptoms such as syncope, chest pain, or EKG changes should be admitted for parenteral antibiotic therapy and cardiac monitoring. The most common manifestation of Lyme carditis is AVB. AVB may manifest as first-degree block, or may present as high-grade second or third-degree block. Other manifestations of Lyme carditis may include myopericarditis, left ventricular dysfunction, and cardiomegaly. Resolution of carditis is typically achieved through antibiotic administration, although pacemaker placement should be considered if the PR interval fails to normalize or if higher degrees of heart block, with accompanying symptoms, are encountered. With the rising incidence of LD, providers must maintain a high level of suspicion in order to promptly diagnose and treat Lyme carditis.



Repeat:  Researchers need to refrain from stating that something is “rare” with Lyme disease as:
  • testing misses more than 70% of cases (thousands go undiagnosed)
  • much fewer report the EM rash than is quoted
  • this is still a misunderstood illness that doctors are woefully uneducated on.  If a patient doesn’t present with the EM rash, doctors unfamiliar with the wide symptom presentation are not going to catching this.

For more:

Click on image to see better. The graph is clear that there is a wide range of those with those finding the EM rash. While the EM rash is diagnostic for Lyme disease, many do not get it. In the first ever patient group in Lyme, Connecticut, only a quarter had the rash:

Again, mainstream medicine continues with abysmal testing and ancient dogma that is hurting patients.

More accurate scientific language would be: “Heart palpitations are rarely reported in the literature.”  What happens in the real world is often quite different than what is reported in the literature – particularly with Lyme as research has been hijacked by The Cabal:

BTW: I had chest palpitations, my husband had chest palpitations, and most of the patients I work with have them.  I don’t think it’s nearly as rare as  is being reported.

It’s a good thing this teen was promptly diagnosed as people have died from this: 

The following statement is quite frightening:

The hospital course was further remarkable for transition to 2nd degree heart block and transient episodes of complete heart block.  Excerpt:

In 90% of cases, the most common consequence of Lyme carditis is heart block. The severity of the heart block can fluctuate rapidly and the progression to complete heart block can be fatal. Importantly, the heart block in Lyme carditis can be transient and usually resolves with antibiotic therapy. Additionally, Lyme carditis can affect other parts of the heart’s conduction system, as well as the heart’s muscle, valves, and outer layer of the heart wall.

These links show heart issues caused by Lyme disease are not rare.

Lyme advocate, Phyllis Mervine, makes a case that autopsies should be performed on those with unexpected, sudden death: