Archive for the ‘Lyme’ Category

Antibodies to Bb & Bartonella in Serum and Synovial Fluid in Those With Rheumatic Diseases & Synovectomy for Lyme Arthritis

https://pmc.ncbi.nlm.nih.gov/articles/PMC10986562/

. 2024 Mar 14;12(4):e01653-23. doi: 10.1128/spectrum.01653-23

Antibodies to Borrelia burgdorferi and Bartonella  species in serum and synovial fluid from people with rheumatic diseases

Editor: Anna Moniuszko-Malinowska5
PMCID: PMC10986562  PMID: 38483477
ABSTRACT

Vector-borne infections may underlie some rheumatic diseases, particularly in people with joint effusions. This study aimed to compare serum and synovial fluid antibodies to B. burgdorferi and Bartonella spp. in patients with rheumatic diseases. This observational, cross-sectional study examined paired synovial fluid and serum specimens collected from 110 patients with joint effusion between October 2017 and January 2022. Testing for antibodies to B. burgdorferi (using CDC criteria) and Bartonella spp. via two indirect fluorescent antibody (IFA) assays was performed as part of routine patient care at the Institute for Specialized Medicine (San Diego, CA, USA). There were 30 participants (27%) with positive two-tier B. burgdorferi serology and 26 participants (24%) with IFA seroreactivity (≥1:256) to B. henselae and/or B. quintana. Both B. burgdorferi IgM and IgG were detected more frequently in synovial fluid than serum: 27% of patients were either IgM or IgG positive in synovial fluid, compared to 15.5% in serum (P = 0.048). Conversely, B. henselae and B. quintana antibodies were detected more frequently in serum than synovial fluid; overall only 2% of patients had positive IFA titers in synovial fluid, compared to 24% who had positive IFA titers in serum (P < 0.001). There were no significant associations between B. burgdorferi or Bartonella spp. seroreactivity with any of the clinical rheumatological diagnoses. This study provides preliminary support for the importance of synovial fluid antibody testing for documenting exposure to B. burgdorferi but not for documenting exposure to Bartonella spp.

https://danielcameronmd.com/what-do-i-do-when-specialists-disagree/

Synovectomy for Lyme Arthritis

She had been ill for nearly two years when synovectomy for Lyme arthritis was recommended.

Her knee remained swollen, painful, and limiting despite treatment for Lyme arthritis. She had completed antibiotic therapy. When the swelling persisted, she was told the infection had been treated and what remained was inflammation.

Surgery was presented as the next step.

What was not discussed was how limited the supporting evidence actually is.


What Synovectomy Does—and Does Not Do

A synovectomy removes inflamed synovial tissue, most commonly from the knee. In some inflammatory arthritides, this can reduce swelling and improve joint function.

In synovectomy for Lyme arthritis, the procedure addresses local joint inflammation only. It does not treat Lyme disease systemically and has not been shown to prevent persistent or recurrent tick-borne infection in other organs.


The Evidence Supporting Synovectomy for Lyme Arthritis

The evidence supporting synovectomy for Lyme arthritis is narrow.

It rests primarily on a small case series published more than three decades ago involving patients with persistent knee effusions after antibiotic therapy. There are no large contemporary trials and no studies demonstrating that synovectomy alters the overall course of Lyme disease or prevents disease persistence outside the joint.

This context should be part of informed consent—but often isn’t.


Symptoms Beyond the Joint

Although the treatment plan focused on her knee, her illness extended beyond a single joint.

She experienced fatigue, cognitive slowing, and generalized symptoms that did not fit neatly into a surgical framework. These symptoms were not addressed in surgical discussions, despite their impact on daily function.


What Happened After Delay

After a period of delay, she was retreated medically.

Her improvement was gradual but meaningful. Over time, systemic symptoms eased and function improved—despite the prolonged course and delayed intervention.


Clinical Experience with Complex Lyme Arthritis Cases

In my practice, I see patients who have been told their joint inflammation is purely post-infectious, even when systemic symptoms suggest a broader process. Synovectomy may help select patients with truly isolated, refractory synovitis. But when symptoms extend beyond the joint, a careful re-evaluation—and, in some cases, medical retreatment—can be more clinically meaningful than focusing solely on tissue removal.

The decision should be based on the whole patient, not just the inflamed joint.


What Was Missing

A complete discussion would have made clear that synovectomy is a procedure aimed at reducing local joint inflammation, not at treating Lyme disease itself. It would have acknowledged that surgery has not been shown to prevent persistent or recurrent tick-borne infection elsewhere in the body, including the nervous system or other organs.

It also would have explained that the evidence supporting synovectomy in Lyme arthritis is limited, based largely on a small, decades-old case series rather than modern comparative trials. Importantly, it would have emphasized that even after prolonged symptoms, other medical options may still be appropriate, particularly when the clinical picture extends beyond a single joint.

Without this context—without an honest discussion of what is known, what is uncertain, and what alternatives remain—patients cannot fully understand their choices. And without that understanding, consent cannot truly be considered informed.


❓ Common Questions Patients Ask About Synovectomy for Lyme Arthritis

Does synovectomy cure Lyme disease?
No. Synovectomy does not cure Lyme disease. It removes inflamed tissue from a joint but does not treat infection elsewhere in the body.

Is there strong scientific evidence supporting synovectomy for Lyme arthritis?
No. The evidence is limited and largely based on a small case series published in the early 1990s. There are no modern randomized trials.

Can synovectomy prevent persistent Lyme infection in other organs?
No studies have shown that synovectomy prevents persistent or recurrent tick-borne infection in the nervous system, heart, or other tissues.


🩺 Clinician Perspective

Most patients with Lyme arthritis improve with antibiotics. A smaller subset develops persistent joint inflammation. In carefully selected cases, synovectomy may reduce localized synovitis.

However, the evidence remains limited, and the procedure has not been shown to alter systemic Lyme disease or prevent persistent infection in other tissues. Ethical care requires that these limits be disclosed as part of informed consent.

Resources
  1. Lochhead RB, et al. Post-infectious Lyme arthritis and immune-mediated synovitis. Clin Rev Allergy Immunol.
  2. Schoen RT, et al. Arthroscopic synovectomy in antibiotic-refractory Lyme arthritis. Arthritis Rheum. 1991.
  3. CDC. Signs and Symptoms of Untreated Lyme Disease
  4. Dr. Daniel Cameron: Lyme Science Blog. Signs and symptoms of Lyme disease
  5. Dr. Daniel Cameron: Lyme Science Blog. Lyme Disease Symptoms

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For more:

Persistent Infection, Molecular Mimicry, and the Future of Chronic Lyme

http://  Approx. 1.5 Hours

Tick Boot Camp

3/14/26I

(https://tickbootcamp.com/podcast/), host Matt Sabatello is joined by Amy Proal, PhD, a leading microbiologist and one of the most influential scientific voices reshaping how chronic Lyme disease and tick-borne illness are understood.

Dr. Proal is the President and Research Director of the PolyBio Research Foundation and serves as Scientific Director of the Cohen Center for Recovery from Complex Chronic Illness at Mount Sinai, where research and clinical care intersect to advance treatment for patients with complex post-infectious disease.

This conversation dives deep into why many Lyme patients remain sick long after standard treatment, exploring the concept of persistent infection and how pathogens like Borrelia can evade immune detection by hiding in tissue rather than circulating in blood.

Dr. Proal explains why conventional blood tests often fail, why chronic illness must be studied at the tissue level, and how new diagnostic technologies may finally uncover what has been missed for decades.

Matt and Dr. Proal also explore molecular mimicry, a mechanism in which pathogens trigger autoimmune-like symptoms by producing proteins that resemble human tissue, leading the immune system to attack both the infection and the body itself. They discuss why immune suppression may temporarily reduce symptoms while allowing infection to persist, and why supporting immune function is often a critical piece of long-term healing.

The episode further examines the idea of successive infection, where cumulative infections, environmental exposures, and physical injuries such as concussions progressively dysregulate the immune system, explaining why some people become severely ill from Lyme disease while others do not.

Dr. Proal also sheds light on neurological Lyme disease, the role of the vagus nerve, and how infections outside the brain can still drive profound neurological and autonomic symptoms.

Throughout the discussion, Dr. Proal shares how her own experience with chronic illness shaped her scientific career and why patient-centered research is essential for meaningful progress.

This episode offers validation, clarity, and hope for anyone affected by chronic Lyme disease and tick-borne illness, and highlights the scientific momentum finally pushing the field toward better diagnostics, targeted treatments, and real answers.

To learn more about Amy Proal’s work, visit PolyBio Research Foundation and the Cohen Center for Recovery from Complex Chronic Illness.

For more:

 

 

 

 

 

Lyme Disease Coinfections & the Brain

http://

Feb 26, 2026
Clinical Strategies for Neuropsychiatric and Neurological Recovery
Join Dr. Aylin Ozdemir for an expert-led exploration of the neurological and neuropsychiatric complexities of Lyme disease and associated co-infections, based on a recently published peer-reviewed research paper (June 2025).
This webinar examines why Lyme disease is frequently misdiagnosed in patients presenting with cognitive, behavioural, and neurological symptoms, and how expanded diagnostic approaches can reveal underlying immune dysregulation and neuroinflammation when standard testing falls short.
Drawing from real-world clinical cases, viewers will learn about integrative therapeutic approaches to support neurological and neuropsychiatric recovery. We’ll explore practical strategies to better recognise, treat, and support recovery in complex neuro-Lyme presentations:
Why Lyme disease often presents as psychiatric or neurological illness The limitations of standard testing How expanded diagnostics improve detection Clinical insight: Real-world case examples Recognising complex neuropsychiatric presentations Integrative therapeutic approaches: Antimicrobial strategies Immune modulation Neuroprotective and mitochondrial support Long-term maintenance protocols to help reduce relapse Dr. Kunal Garg provides a brief overview of the application of CARE Guidelines, highlighting the importance of rigorous case documentation and high-quality publishing in advancing evidence-informed Lyme disease care.
For more:

Bartonella and Borrelia-Related Disease Presenting as a Neurological Condition Revealing the Need for Better Diagnostics

https://www.mdpi.com/2076-2607/12/1/209

Bartonella and Borrelia-Related Disease Presenting as a Neurological Condition Revealing the Need for Better Diagnostics

by Marna E. Ericson1, B. Robert Mozayeni1, Laurie Radovsky2 and Lynne T. Bemis3,*
1T Lab Inc., Gaithersburg, MD 20878, USA
2Laurie Radovsky, M.D. LLC., St. Paul, MN 55102, USA
3Department of Biomedical Sciences, Medical School Duluth Campus, University of Minnesota, Duluth, MN 55812, USA
*Author to whom correspondence should be addressed.
Microorganisms 202412(1), 209; https://doi.org/10.3390/microorganisms12010209
Submission received: 21 December 2023 / Revised: 16 January 2024 / Accepted: 18 January 2024 / Published: 19 January 2024
(This article belongs to the Special Issue Bartonella and Bartonellosis: New Advances and Further Challenges)

Abstract

The diagnostic tests available to identify vector-borne pathogens have major limitations. Clinicians must consider an assortment of often diverse symptoms to decide what pathogen or pathogens to suspect and test for. Even then, there are limitations to the currently available indirect detection methods, such as serology, or direct detection methods such as molecular tests with or without culture enrichment. Bartonella spp., which are considered stealth pathogens, are particularly difficult to detect and diagnose. We present a case report of a patient who experienced a spider bite followed by myalgia, lymphadenopathy, and trouble sleeping. She did not test positive for Bartonella spp. through clinically available testing. Her symptoms progressed and she was told she needed a double hip replacement. Prior to the surgery, her blood was submitted for novel molecular testing, where Bartonella spp. was confirmed, and a spirochete was also detected. Additional testing using novel methods over a period of five years found Bartonella henselae and Borrelia burgdorferi in her blood.
This patient’s case is an example of why new diagnostic methods for vector-borne pathogens are urgently needed and why new knowledge of the variable manifestations of Bartonellosis need to be provided to the medical community to inform and heighten their index of suspicion.
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**Comment**
You will recognize Marna Ericson’s name as her son had a severe bartonella infection.  She managed to take advanced imaging techniques on samples and found Bartonella alive and well in tissues surrounding where a PIC line had been removed.  She has teamed up with other researchers investigating Bartonella.  We can be extremely thankful for their work.
For more:

The Great Alzheimer’s Scam & the Proven Cures They’ve Buried For Billions

https://www.midwesterndoctor.com/p/the-great-alzheimers-scam-and-the

The Great Alzheimer’s Scam and The Proven Cures They’ve Buried for Billions

Decades of neglect in understanding the actual causes of dementia have transformed it into one of the most costly diseases in existence.

• Alzheimer’s disease is commonly thought to result from abnormal plaque buildup in the brain that gradually destroys brain tissue. As a result, almost all Alzheimer’s research has been directed toward eliminating amyloid, even after the basis for much of this work was shown to stem from fraudulent research.

•As such, despite decades of research and billions of dollars spent, this model has completely failed to produce useful results. The costly “groundbreaking” Alzheimer’s drugs only slightly slow dementia progression—at the expense of causing brain bleeding and swelling in over a quarter of those treated.

•In contrast, numerous affordable treatments have been developed for Alzheimer’s disease that target the root causes of the disorder, producing significant benefits at a fraction of the cost and without any toxicity.

•One neurologist, for example, proposed that amyloid serves a protective function in the brain and treats Alzheimer’s by identifying the underlying process causing dementia (which can often be diagnosed through symptoms). Remarkably, despite the method being proven in clinical research, awareness of it or the fact there are completely different types of “Alzheimer’s disease” which require different treatments remains almost nonexistent.

•Likewise, a strong case can be made that impaired cerebral circulation, along with impaired venous and lymphatic drainage, plays a pivotal role in Alzheimer’s disease.

•This article will review the common causes of cognitive impairment and dementia (e.g., cells becoming trapped in a shocked state where they no longer function) along with the forgotten treatments for neurodegenerative disorders—some of which, like DMSO, have extensive evidence supporting their use.

Dr. Dale Bredesen detailed in The End of Alzheimer’s, a few pivotal conclusions:

  • Amyloid protein is a protective mechanism the brain uses to protect itself from other stressors that endanger brain tissue.
  • Rather than there being one type of Alzheimer’s, there are actually three with different symptoms, and it is essential to recognize which type someone has before initiating treatment.
    • Type 1: Inflammatory – often metabolic or infectious
      • Type 1.5 Glycotoxic (hybrid of types 1&2) insulin resistance and chronically elevated blood sugar
    • Type 2: Atrophic – deficiences in nutrients, hormones, and other factors
    • Type 3: Toxic – exposure to mold, chronic infections such as Lyme disease, Herpesvirus, cytomegalovirus, fungal infections, etc. heavy metals, and household chemicals
    • Type 4: Vascular – hypertension, atherosclerosis, or anything causing chronic restriction of cerebral blood flow
    • Type 5: Traumatic – brain injury
  • The brain is designed to be able to adapt to the needs of life, so it is always creating or pruning neural connections and brain cells. Alzheimer’s, in turn, results from the loss of signals that sustain brain cells, and the dismantling of neural connections outweighing the formation of new ones, gradually compounding over the decades.

As such, his formula was fairly straightforward: identify the type of Alzheimer’s someone has, eliminate its causes, and gradually wait for the physiological momentum to shift from neurodegeneration to neurodevelopment.  (See link for article)

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**Comment**

Many anecdotal reports of using DMSO successfully for dementia are given in the article.

For more: