Archive for the ‘Lyme’ Category

Lyme Disease Leads to Muscle Weakness of the Leg & Constipation

https://danielcameronmd.com/lyme-disease-muscle-weakness-of-the-leg-and-constipation/

LYME DISEASE LEADS TO MUSCLE WEAKNESS OF THE LEG AND CONSTIPATION

lyme-disease-muscle-weakness

In their article, “Atypical Acute Neuroborreliosis With Leg Paresis and Constipation,” Ahrend and colleagues describe a case of Lyme disease presenting with neurological and autonomic manifestations in an elderly man. [1]

By 

An 80-year-old man, later diagnosed with Lyme disease, was admitted to the hospital with left leg paresis [muscle weakness], along with pain and sensory disturbances in his left abdomen. He also had a rash on his left lower abdomen, severe abdominal pain and constipation. The symptoms had been ongoing for 4-5 weeks.

The patient had visited three other medical centers for evaluation of his abdominal pain. However, a colonoscopy and CT scan of the abdomen did not explain the severity of the patient’s symptoms.

The rash manifest as a “patchy, pruritic redness with pustules, which was particularly prominent on the left flank and abdomen,” the authors state.

Testing for Lyme disease revealed Borrelia-specific IgM and IgG antibodies, consistent with the symptomatology of neuroborreliosis.

“Finally, a diagnosis of [Lyme disease] was made, which initially manifested itself with autonomic symptoms (constipation) and severe abdominal pain, accompanied by a skin rash” and muscle weakness in his left leg that appeared later on, the authors state.

“The patient’s constipation is likely due to the autonomic involvement of the disease.”

The rash, characterized as a flat, itchy redness with pustules, was atypical for Lyme disease, the authors point out.

“… serological tests were finally conclusive for Lyme borreliosis, so that the abdominal pain and [constipation] were evaluated as autonomic, and the leg paresis as neurological involvement of neuroborreliosis.”

The patient’s symptoms resolved completely following a 21-day course of doxycycline.

After treatment for Lyme disease, the patient’s muscle weakness disappeared, as did his intestinal symptoms. And, he was able to “resume his home exercise program within two months and since then he has been on the same physical level as before,” the authors state.

References:
  1. Ahrend H, Fibbe C, Jasper D, Ahrend A, Woelfel M, Layer P, Rosien U, Stope MB. Atypical Acute Neuroborreliosis With Leg Paresis and Constipation. In Vivo. 2024 Mar-Apr;38(2):940-943. doi: 10.21873/invivo.13523. PMID: 38418126; PMCID: PMC10905454.
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**Comment**
This patient requires a follow-up.
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Category:

Lyme, research, Testing

A Protein Found in Human Sweat May Protect Against Lyme Disease

https://www.lymedisease.org/human-sweat-lyme-disease/

A protein found in human sweat may protect against Lyme disease

By Anne Trafton, MIT News

Lyme disease, a bacterial infection transmitted by ticks, affects nearly half a million people in the United States every year. In most cases, antibiotics effectively clear the infection, but for some patients, symptoms linger for months or years.

Researchers at MIT and the University of Helsinki have now discovered that human sweat contains a protein that can protect against Lyme disease. They also found that about one-third of the population carries a genetic variant of this protein that is associated with Lyme disease in genome-wide association studies.

It’s unknown exactly how the protein inhibits the growth of the bacteria that cause Lyme disease. However, the researchers hope to harness the protein’s protective abilities to create skin creams that could help prevent the disease, or to treat infections that don’t respond to antibiotics.

“This protein may provide some protection from Lyme disease, and we think there are real implications here for a preventative and possibly a therapeutic based on this protein,” says Michal Caspi Tal. She’s a principal research scientist in MIT’s Department of Biological Engineering and one of the senior authors of the new study.

Hanna Ollila, a senior researcher at the Institute for Molecular Medicine at the University of Helsinki and a researcher at the Broad Institute of MIT and Harvard, is also a senior author of the paper, which has been published in Nature Communications. The paper’s lead author is Satu Strausz, a postdoc at the Institute for Molecular Medicine at the University of Helsinki.

A surprising link

Lyme disease is most often caused by a bacterium called Borrelia burgdorferi. In the United States, this bacterium is spread by ticks that are carried by mice, deer, and other animals. Symptoms include fever, headache, fatigue, and a distinctive bull’s-eye rash.

Most patients receive doxycycline, an antibiotic that usually clears up the infection. In some patients, however, symptoms such as fatigue, memory problems, sleep disruption, and body aches can persist for months or years.

Tal and Ollila, who were postdocs together at Stanford University, began this study a few years ago in hopes of finding genetic markers of susceptibility to Lyme disease. To that end, they decided to run a genome-wide association study (GWAS) on a Finnish dataset that contains genome sequences for 410,000 people, along with detailed information on their medical histories.

This dataset includes about 7,000 people who had been diagnosed with Lyme disease, allowing the researchers to look for genetic variants that were more frequently found in people who had had Lyme disease, compared with those who hadn’t.

Secretoglobin

This analysis revealed three hits, including two found in immune molecules that had been previously linked with Lyme disease. However, their third hit was a complete surprise — a secretoglobin called SCGB1D2.

Secretoglobins are a family of proteins found in tissues that line the lungs and other organs, where they play a role in immune responses to infection. The researchers discovered that this particular secretoglobin is produced primarily by cells in the sweat glands.

To find out how this protein might influence Lyme disease, the researchers created normal and mutated versions of SCGB1D2 and exposed them to Borrelia burgdorferi grown in the lab.

They found that the normal version of the protein significantly inhibited the growth of Borrelia burgdorferi. However, when they exposed bacteria to the mutated version, twice as much protein was required to suppress bacterial growth.

The researchers then exposed bacteria to either the normal or mutated variant of SCGB1D2 and injected them into mice. Mice injected with the bacteria exposed to the mutant protein became infected with Lyme disease, but mice injected with bacteria exposed to the normal version of SCGB1D2 did not.

“In the paper we show they stayed healthy until day 10, but we followed the mice for over a month, and they never got infected. This wasn’t a delay, this was a full stop. That was really exciting,” Tal says.

Preventing infection

After the MIT and University of Helsinki researchers posted their initial findings on a preprint server, researchers in Estonia replicated the results of the genome-wide association study, using data from the Estonian Biobank. These data, from about 210,000 people, including 18,000 with Lyme disease, were later added to the final Nature Communications study.

The researchers aren’t sure yet how SCGB1D2 inhibits bacterial growth, or why the variant is less effective. However, they did find that the variant causes a shift from the amino acid proline to leucine, which may interfere with the formation of a helix found in the normal version.

They now plan to investigate whether applying the protein to the skin of mice, which do not naturally produce SCGB1D2, could prevent them from being infected by Borrelia burgdorferi. They also plan to explore the protein’s potential as a treatment for infections that don’t respond to antibiotics.

“We have fantastic antibiotics that work for 90 percent of people, but in the 40 years we’ve known about Lyme disease, we have not budged that,” Tal says. “Ten percent of people don’t recover after having antibiotics, and there’s no treatment for them.”

A new approach to Lyme prevention?

“This finding opens the door to a completely new approach to preventing Lyme disease in the first place, and it will be interesting to see if it could be useful for preventing other types of skin infections too,” says Kara Spiller, a professor of biomedical innovation in the School of Biomedical Engineering at Drexel University, who was not involved in the study.

The researchers note that people who have the protective version of SCGB1D2 can still develop Lyme disease, and they should not assume that they won’t. One factor that may play a role is whether the person happens to be sweating when they’re bitten by a tick carrying Borrelia burgdorferi.

SCGB1D2 is just one of 11 secretoglobin proteins produced by the human body. Tal also plans to study what some of those other secretoglobins may be doing in the body, especially in the lungs, where many of them are found.

“The thing I’m most excited about is this idea that secretoglobins might be a class of antimicrobial proteins that we haven’t thought about. As immunologists, we talk nonstop about immunoglobulins, but I had never heard of a secretoglobin before this popped up in our GWAS study. This is why it’s so fun for me now. I want to know what they all do,” she says.

The research was funded, in part, by Emily and Malcolm Fairbairn, the Instrumentarium Science Foundation, the Academy of Finland, the Finnish Medical Foundation, the Younger Family, and the Bay Area Lyme Foundation.

Click here to read the study.

SOURCE: Massachusetts Institute of Technology

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**Comment**

These mice need to be observed for years, not 10 or even 30 days.

The most inaccurate statement in the article:

“We have fantastic antibiotics that work for 90 percent of people, but in the 40 years we’ve known about Lyme disease, we have not budged that,” Tal says. “Ten percent of people don’t recover after having antibiotics, and there’s no treatment for them.”

She’s right about not moving forward, but this 10% going onto suffer with chronic symptoms is flat-out wrong and needs to be corrected.  We also don’t have ‘fantastic antibiotics.’  We have a lot yet to learn about this complex illness due to a highly connected cabal with histories with biological weapons doing all the research utilizing faulty study designs.

For far too long this cabal has treated this as a mono-infection cured by a mono-therapy and nothing could be further from the truth.  There is absolutely nothing about this beast that is straight forward or easy, except the continued propaganda.

Category:

Lyme, research

Concurrent Infection of the Human Brain With Multiple Borrelia Species

https://www.mdpi.com/1422-0067/24/23/16906

Concurrent Infection of the Human Brain with Multiple Borrelia Species

by  1,*, 2,3, 1,3, 2,3, 4, 4, 5, 6, 6 and 1,*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2023, 24(23), 16906; https://doi.org/10.3390/ijms242316906
Submission received: 10 October 2023 / Revised: 22 November 2023 / Accepted: 26 November 2023 / Published: 29 November 2023
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)

Abstract

Lyme disease (LD) spirochetes are well known to be able to disseminate into the tissues of infected hosts, including humans. The diverse strategies used by spirochetes to avoid the host immune system and persist in the host include active immune suppression, induction of immune tolerance, phase and antigenic variation, intracellular seclusion, changing of morphological and physiological state in varying environments, formation of biofilms and persistent forms, and, importantly, incursion into immune-privileged sites such as the brain. Invasion of immune-privileged sites allows the spirochetes to not only escape from the host immune system but can also reduce the efficacy of antibiotic therapy. Here we present a case of the detection of spirochetal DNA in multiple loci in a LD patient’s post-mortem brain. The presence of co-infection with Borrelia burgdorferi sensu stricto and Borrelia garinii in this LD patient’s brain was confirmed by PCR. Even though both spirochete species were simultaneously present in human brain tissue, the brain regions where the two species were detected were different and non-overlapping. The presence of atypical spirochete morphology was noted by immunohistochemistry of the brain samples. Atypical morphology was also found in the tissues of experimentally infected mice, which were used as a control.
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‘The powers that be’ continue to ignore the issue of coinfection and concurrent infection.  This is a huge problem that partially explains why patients remain sick after the extremely unscientific and antiquated CDC Lyme treatment.

Category:

Lyme, research

Tackling Long-Haul Diseases

https://www.technologyreview.com/2024/02/28/1087617/tackling-long-haul-diseases/

Tackling long-haul diseases

Long-haul covid and chronic Lyme disease are surprisingly similar. MIT immunoengineer Mikki Tal is on the case.
Allison Guy, SM ’23archive page
February 28, 2024

MIT immunoengineer Michal “Mikki” Tal remembers the exact moment she had an insight that would change the trajectory of her research, getting her hooked on studying a long-neglected disease that leaves millions of Americans suffering without treatment.

It was 2017, and she was a Stanford postdoc exploring connections between her immune regulation research and immuno-oncology, which harnesses the body’s immune system to combat cancer. Her work focused on how healthy cells broadcast “Don’t eat me” messages while cells that are cancerous or infected with a pathogen send self-sacrificing “Eat me” messages. Immune cells, in turn, receive these missives in pocket-like receptors. The receptor that receives the healthy cells’ signal, Tal read as she was poring over the literature that day, is the third most diverse protein in the human population, meaning that it varies a lot from one person to the next. It was a fact that struck her as “very odd.”

Tal, who has been obsessed with infectious disease since losing an uncle to HIV/AIDS and a cousin to meningococcal meningitis, wondered what this striking diversity could reveal about our immune response to infection. According to one hypothesis, the wide array of these receptors is the result of an evolutionary arms race between disease-causing microbes and the immune system. Think of the receptor as a lock, and the “Nothing to see here” message as a key. Pathogens might evolve to produce their own chemical mimics of this key, effectively hiding from the immune system in plain sight. In response, the human population has developed a wide range of locks to frustrate any given impostor key.

Wanting to test this hypothesis, Tal found herself walking the halls of Stanford, asking colleagues, “Who’s got a cool bug?” Someone gave her Borrelia burgdorferi, the bacterium that causes Lyme disease. Previous research from Tal’s collaborator Jenifer Coburn, a microbiologist now at the Medical College of Wisconsin, had established that Lyme bacteria sport a special protein crucial for establishing a lasting infection. Knock this protein out, and the immune system swiftly overwhelms the bugs. The big question, however, was what made this protein so essential. So Tal used what’s known as a high-affinity probe as bait—and caught the Borrelia’s mimic of our “Don’t eat me” signal binding to it. In other words, she confirmed that the bacteria’s sneaky protein was, as predicted, a close match for a healthy cell’s signal.  (See link for article)

“Long covid looks exactly, and I mean exactly, like chronic Lyme.” ~ Michal “Mikki” Tal, MIT immunoengineer

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**Comment**

Yet, despite knowing of this ‘sneaky protein’ that establishes a lasting infection, ‘the powers that be’ deny chronic/persistent illness with Lyme/MSIDS.

 While the article factually states there’s no objective way to diagnose chronic Lyme and no medically ‘accepted’ therapy, it regurgitates the ‘same o, same o’ myth that only 10% suffer chronic symptoms.
It also correctly points out that short-term doxycycline, the widely ‘accepted’ treatment for Lyme, only prevents the bacteria from replicating which relies upon the immune system to kill off invaders which often doesn’t work due to the fact Lyme effectively gives patients immune system dysfunction – rendering it virtually useless. The article states that lengthy antibiotics can “ease” symptoms.  I would disagree with this.  For a subset of patients, it makes them completely well.
Predictably coinfection involvement is entirely missing from the conversation.
The author is far more into gender differences, which is the buzz word of the day, matters little, and won’t matter a tittle in helping patients get better.  This ‘flavor of the day’ approach to research is the new norm and is unfortunately now required to get coveted government grants.  All researchers know this little factoid, but the public remains in the dark.
Complaint aside, I did find the mouse experiment extremely interesting as it showed how Lyme ‘completely disfigured’ the uterus, which would explain why so many infected women have difficulties with pregnancies.  Only ONE other study in the history of Lyme documented uterine infection.
This does show the extremely limited and biased approach to all things Lyme/MSIDS and it always amazes me that researchers literally have to stumble into this knowledge.
Blaming men is not the answer regarding the problems in research. The problem stems from conflicts of interest and corruption – with females just as culpable as males.
While gender differences might be interesting, even illuminating, there are far bigger fish to fry in the Lyme/MSIDS kitchen.
The article then switches gears into Long COVID, a contested term that has yet to be proven conclusively, yet accepted at face value by many.  The first thing that crosses my mind when I hear that “Long COVID” and Lyme have identical symptoms is, who’s to say it isn’t Lyme?  
Testing for both diseases is abysmal, and seriously comical if lives weren’t at stake.  Yet, testing by ‘the powers that be’ simply is and continues to be accepted and utilized.
The article then gives the hypothesis dichotomy:
  1. persistent pathogens drive ongoing symptoms
  2. the immune system remains in a faulty state – driving symptoms

Tal’s project uses AI which she hopes will allow her to predict who will go on to have persistent symptoms.  She has already learned that current Lyme tests only look at IgG and IgM – not IgE, which she describes as an immune system ‘air strike’ and that those with this type of immune reaction have been ignored in research.  She received $2 million to further test this hypothesis and she expects to publish findings as early as 2025.

And hold the press! – Tal states that at a conference the keynote speaker actually apologized for what he had written in the past about chronic Lyme after he got ‘Long COVID.’

Sadly, right after this, the article predictably blames ‘climate change’ for pushing ticks into new habitats – a notion refuted by independent research, as well as more and more climate scientists, and more and more data proving there is no ‘climate emergency,’ but how the media is using corrupt data to push a narrative pushed by the UN which is bankrolling politics under a ‘climate change’ narrative.  ‘Climate change’ is big, big business, and part of a much larger agenda which utilizes science and technology for ultimate control.

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Category:

Lyme, research, Testing, Ticks, Viruses

Can Lyme Disease Cause Speech Issues?

https://danielcameronmd.com/can-lyme-disease-cause-speech-issues/

CAN LYME DISEASE CAUSE SPEECH ISSUES?

Can-Lyme-cause-speech-issues

“Lyme can affect the nerves that are responsible for controlling the muscles in the vocal cords,” says Amesh A. Adalja, MD, an infectious disease specialist at Johns Hopkins Center for Health Security. “As a result, someone could technically lose their voice if they had Lyme disease.”

By 

“Lyme disease has been associated with a wide variety of persistent neuropsychological and cognitive symptoms, including: impaired attention, focus, concentration, judgment, and impulse control,” in addition to impaired memory and speech functions, according to an article published by Amen Clinics.¹

Recent studies of patients with post-treatment Lyme disease syndrome (PTLDS) have found “consistent deficits in memory and processing speed,” according to the authors of a new study “Language Fluency Deficits in Post-treatment Lyme Disease Syndrome.”² But are language fluency deficits due to poor performance in these other neurocognitive areas?

The study by Gorlyn et al. evaluated 38 individuals with major depressive disorder (MDD), 59 healthy volunteers, and 31 individuals with Post-treatment Lyme disease Syndrome (PTLDS).

The major depressive disorder group “had a cumulative time since first episode of depression of 13.5 ± 10.9 years, with an average 3.8 ± 3.5 episodes of depression,” wrote Gorlyn et al.

The Post-treatment Lyme Disease Syndrome group “had a duration of illness of 7.7 ± 5.6 years of illness and had gone 13.0 ± 18.5 (median = 7.0) months before being formally diagnosed and treated for Lyme disease.”

Additionally, the PTLDS group “received an average of 2.3 ± 1.7 months of prior intravenous antibiotic treatment and 7.4 ± 9.8 (median = 3) months of prior oral antibiotic treatment.”

The study found that both the PTLDS and MDD groups had deficits in basic verbal abilities, memory, and processing speed.

“…language fluency deficits were evident in PTLDS patients even after controlling for the significant effects of verbal ability, slowed processing speed, and memory difficulties on fluency performance.”

The authors concluded, “Language fluency appears to be an independent area of neurocognitive deficit within the constellation of PTLDS symptoms.”

These deficits in language fluency could not be a function of depressed mood, basic verbal abilities, or other cognitive problems, the authors point out.

“These findings suggest that language problems are a distinct area of cognitive deficit in PTLDS, and not a function of depressed mood, basic verbal abilities, or other cognitive problems frequently observed in PTLDS.”

The findings support those from other studies. “A clearer picture of these patients’ neurocognitive difficulties has emerged incorporating mild slowing, disruptions of learning and information retrieval, and dysfunction in everyday language skills,” wrote the authors.

The study was not designed to determine if the language fluency deficits in Lyme disease were transient or a long-standing effect, although the PTLDS group had been ill for years despite antibiotic treatment. Nor was the study designed to determine the cause of the language fluency deficits in Lyme disease.

References:
  1. Amen Clinics. November 15, 2022. https://rb.gy/ac4geu
  2. Gorlyn M, Keilp JG, Fallon BA. Language Fluency Deficits in Post-treatment Lyme Disease Syndrome. Arch Clin Neuropsychol. Dec 22 2022;doi:10.1093/arclin/acac095

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Category:

Lyme, research