Archive for the ‘Biofilm’ Category

Can These Essential Oils Help Lyme Patients Overcome Chronic Candida?

https://www.linkedin.com/pulse/can-essential-oils-help-lyme-disease-patients-overcome-greg-lee/

Can These Essential Oils Help Lyme Disease Patients Overcome Chronic Candida Infections?

By Greg Lee Published on

FREE-Sample-of-Essential-Oils

photo credit:  freebiesdip.com

For people diagnosed with Lyme disease that have persistent Candida infections

Have you ever been frustrated by a really slow computer? A month ago, I was making a video and it took f-o-r-e-v-e-r to edit the final version. The computer was being choked by a group of programs called “Bloatware.” These programs ate up huge amounts of disk space and processing which turned my computer into a slow moving tortoise.

How is Bloatware that slows down your computer similar to recurring Candida infections in people also diagnosed with Lyme disease?

Just like Bloatware, Candida can slow you down by eating up your valuable energy and increasing inflammation

According to the US Centers for Disease Control (CDC), Candida lives on the skin and in the digestive tract without normally causing symptoms. Candida can cause local infections in the mouth, throat, esophagus and in the vagina. Candida can also cause systemic infections which affect the blood, heart, brain, eyes, bones, and other parts of the body1. Symptoms found in persistent Candida infections can include leaky gut, irritable bowel syndrome2, chronic fatigue3, arthritis4, clinical depression5, cerebral abscesses6, neck stiffness, seizures7, fever, chills, weakness, and death8. An immune system weakened by Lyme disease may make people more vulnerable to Candida infections.

Lyme disease patients may be more susceptible to recurring Candida infections 

A Lyme disease infection may weaken the immune system and make people more susceptible to opportunistic Candida infections9. Also, many Lyme patients receive prolonged antibiotic therapy which can kill off healthy gut microbes and can lead to irritable bowel syndrome (IBS), leaky gut and Candida overgrowth10. Another theory for chronic Candida in Lyme patients is an inability to produce the necessary inflammatory compounds for eliminating yeast infections.

Chronic Candida infection patients may not be able to produce important anti-fungal inflammatory compounds

In a UK study on chronic Candida infection patients, Interleukin-2 (IL-2), Interleukin-12 (IL-12) production was significantly lower and Interleukin-6 (IL-6) production was much higher11. The study indicates that Candida patients over produce IL-6 which can lead to decreased IL-12. Lower IL-12 is correlated with the inability to clear fungal infections. Patients with gastrointestinal Candida have higher levels of Interleukin-17 (IL-17) which promotes fungal colonization12. Not only Candida, but also Lyme infections can lead to excess inflammation production.

Excess inflammatory compounds may also prevent clearing of Lyme as well as Candida

Increased IL-6 leading to decreased levels of IL-12 may enable Lyme and Candida infections to persist. In neurological Lyme patients, higher levels of inflammatory compounds including IL-6, IL-2, Interleukin-5 (IL-5), Interleukin-10 (IL-10), and CXCL13 were found in spinal fluid13. In a Borrelia infected mice study, decreased IL-12 lead to decreased arthritis and increased levels of Lyme disease in tissues14. In another study, increased IL-17 led to the development of destructive arthritis in mice infected with Borrelia15. Drug resistant strains of Candida may also lead to persistent yeast infections in Lyme patients.

Candida can persist despite multiple anti-fungal medications

In the US and Canada, multi-drug resistant strains of Candida have been found in immune compromised patients16. Candida can also produce a protective slime called a “biofilm” which may make infections up to 1000x more drug resistant17. As a result of resistant and biofilm forms of Candida, Lyme patients undergoing antibiotic therapy may experience recurring Candida infections.

Are there natural remedies that can help to reduce recurring symptoms by targeting antibiotic resistant and biofilm forms of Candida?

Fortunately, there are five essential oils that have been effective against drug resistant and biofilm forms of Candida

In a multiple studies, essential oils were effective at inhibiting drug resistant forms of Candida than anti-fungal medications. Other essential oils were highly effective at reducing Candida biofilms. Many of these essential oils have been used safely for years in our food supply18 and to help patients with Candida and Lyme disease to reduce relapsing symptoms. Microparticle “liposome” essential oils have greater penetration into organs and tissues in animal and lab studies19.

Anti-Drug Resistant Candida Essential Oil #1: Clove Bud

Clove bud essential oil demonstrated considerable anti-fungal properties against Fluconazole-resistant strains of Candida in one lab study20. In another study, clove bud exhibited anti-biofilm activity against Candida species biofilms21. In another lab study, clove bud inhibited IL-6, interleukin-1beta (IL-1β), and IL-1022.

Clove bud essential oil eradicated all Lyme disease persister cells and dissolved biofilms in a lab study23. In multiple animal and lab studies, clove bud oil has also been effective against biofilms produced by Staphylococcus aureus24, E. Coli25, and Aeromonas hydrophila26. In multiple lab studies, clove oil inhibits Salmonella typhimurium, E. coli, B. cereus, Listeria innocua, Morganella morganii, Listeria monocytogenes, Enterobacteriaceae, S. aureus, and Pseudomonas species27. This oil also posses potent anti-fungal properties against Aspergillus flavus28.

Clove bud oil use is cautioned in pregnancy. This oil has anti-coagulant properties and is cautioned with the use of diabetic medications, anticoagulant medications, after major surgery, peptic ulcer, hemophilia, and other bleeding disorders. It may interact with pethidine, MAOIs or SSRIs. It is also cautioned against using this oil on diseased or damaged, or hypersensitive skin, and with children under 2 years old This oil has US Food and Drug Administration (FDA) generally recognized as safe (GRAS) status29. Similar to clove bud oil, tea tree has excellent anti-Candida properties.

Anti-Drug Resistant Candida Essential Oil #2: Tea Tree

In lab studies, tea tree oil inhibited drug resistant Candida strains30 and was effective at inhibiting biofilm growth31. Tea tree oil was also effective against Staphylococcus epidermidis, Escherichia coli, Saccharomyces cerevisiae32, Pseudomonas aeruginosa and its biofilm,33 Aspergillus niger, Aspergillus flavus34, Aspergillus fumigatus, Penicillium chrysogenum35, Mycoplasma pneumoniae, Mycoplasma hominis and Mycoplasma fermentans36, group A streptococcus37, Fusarium graminearum, Fusarium culmorum, Pyrenophora graminea38, Alternaria alternata, Botrytis cinerea and Fusarium oxysporum39 in lab and animal studies.

In an endotoxin lab study, tea tree essential oil was effective at lowering inflammatory compounds IL-1β, IL-6 and IL-1040. In another lab study, tea tree oil decreased IL-2 and increased anti-inflammatory compound IL-441. Caution: some cases have been reported where tea tree oil caused allergic dermatitis when placed on the skin42. In five cases, high doses of this oil internally, 0.5-1.0 ml/kg, have produced central nervous system symptoms of loss of coordination, drowsiness, unconsciousness, diarrhea, and abdominal pain43. Just like tea tree, geranium essential oil has multiple anti-Candida properties.

Anti-Drug Resistant Candida Essential Oil #3: Geranium

In multiple lab studies, geranium oil inhibited Fluconazole resistant Candida strains44 and inhibited multiple Candida species biofilms45. Geranium oil was also effective at significantly decreasing inflammatory compounds IL-6, IL-10, IL-2 and COX-2 levels when exposed to Candida proteins in another lab study46. In a mouse study, this oil inhibited the degranulation of mast cells47.

The use of geranium oil is cautioned with diabetes medications, drugs metabolized by CYP2B6, and has a low risk of skin sensitization48. Just like geranium, savory reduced resistant forms of Candida.

Anti-Drug Resistant Candida Essential Oil #4: Savory

Due to their compositional similarity, winter and summer savory essential oils are grouped together here. In one lab study, winter savory essential oil was highly effective at inhibiting drug resistant strains of Candida glabrata49. In another lab study, summer savory essential oil demonstrated substantial anti-fungal activity against Candida albicans and it’s biofilms50.

Since these oils may inhibit blood clotting; use is cautioned with anticoagulant medications, major surgery, peptic ulcer, hemophilia, other bleeding disorders. Use is also cautioned with diabetic medications, use on mucous membranes due to a moderate risk of irritation and use on hypersensitive, diseased or damaged skin due to a low risk of skin irritation. Use is also cautioned in children under 2 years of age51. Similar to savory, lemon has demonstrated anti-Candida properties.

Anti-Drug Resistant Candida Essential Oil #5: Lemon

In lab studies, lemon essential oil was effective at inhibiting drug-resistant Candida species52. This oil was also 100% effective at reducing a mixed species Candida albicans and E. Coli biofilm53. If applied to the skin, skin must not be exposed to sunlight or sunbed rays for 12 hours54. These essential oils in combination may help to reduce relapsing symptoms caused by drug resistant and biofilm forms of Candida in patients with Lyme disease.

Essential oils may help to reduce recurring symptoms caused by antifungal resistant and biofilm forms of Candida

Similar to deleting the Bloatware off your computer to speed it up, a powerful combination of essential oils may help you to overcome energy draining and relapsing symptoms caused by drug resistant and biofilm forms of Candida. Formulating these remedies into microparticle liposomes may enhance the stability and extend the anti-fungal activity of these essential oils. Since these essential oils have cautions and contraindications on their use, work with a Lyme literate essential oil practitioner to develop a proper, safe, and effective strategy for your condition.

https://madisonarealymesupportgroup.com/2018/01/03/the-invisible-universe-of-the-human-microbiome-msm/

“Recitas, author of ‘The Plan,’ calls MSM the wonder supplement for your gut. It can alleviate allergy symptoms, helps with detoxification, eliminates free radicals, and improves cell permeability. She states that with given time, MSM will start to actually repair damage caused by leaky gut – a common problem with Lyme/MSIDS patients. It can also help the body’s ability to absorb nutrients from food. Many Lyme patients struggle with paralysis of the gut where the muscles of the stomach and intestines stop being efficient. MSM helps this muscle tone as well.”

https://madisonarealymesupportgroup.com/2018/05/15/overview-of-anti-inflammatory-diets/

https://madisonarealymesupportgroup.com/2017/05/20/minding-your-mitochondria/

https://madisonarealymesupportgroup.com/2018/04/18/comparative-diets-to-address-chronic-inflammation/

 

 

 

 

 

 

 

 

 

 

 

 

 

Lyme Biofilm & Efflux Pumps – Dr. Christine Green

 Approx. 17 Min.

Published on Mar 15, 2018

Dr. Christine Green on Lyme Biofilms and Efflux Pumps

Dr. Christine Green, a Lyme-treating physician who serves on the board of LymeDisease.org, recently spoke on the topic of Lyme biofilms and efflux pumps–two factors that can directly affect treatment for Lyme disease.

https://www.lymedisease.org/green-biofilms-efflux-pumps/

In this second talk, Dr. Green explains how biofilms function within our bodies. A biofilm is a jelly-like barrier created by organisms to protect against environmental stress. There are both healthy biofilms and those that contribute towards illness. The National Institutes of Health (NIH) estimates that 80% of all chronic infections are associated with biofilms.

Research shows that Borrelia burgdorferi, the pathogen that causes Lyme disease, also forms biofilm. This helps protect the bacteria from antibiotics. Adding biofilm busters to antimicrobial treatment may be one way to combat chronic Lyme disease.

In addition to biofilm, Borrelia have something called “efflux pumps” that help the bacteria survive in hostile environments. The efflux pumps push out heavy metals and other chemicals, but they can also expel antibiotics before they’ve had a chance to work. Current research is looking at ways to deal with the problem.

______________

For More:  https://madisonarealymesupportgroup.com/2017/08/18/drexel-prof-lyme-persists/

https://madisonarealymesupportgroup.com/2017/10/26/lyme-wars-part-3/

Great article on biofilm & natural biofilm agents:  https://thescienceofnutrition.me/2015/03/13/natural-anti-biofilm-agents/ (Includes: garlic, NAC, xylitol, coffee, cranberry, enzymes, chelation, & more)

MSM makes cell walls permeable which is why it helps with detoxification and is an important oral chelator:  https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/

 

 

 

 

A Brief History of Neuroborreliosis Research & Dementia – An Inside Look at Two Researchers

https://www.facebook.com/thomas.grier1/posts/10214592863122717?notif_id=1521692245045022&notif_t=notify_me&ref=notif

A Brief History of Neuroborreliosis Research & Dementia – an Inside Look at Two Researchers

Part 1
by
Thomas Grier

Two Ends of the Same Spirochete
How Dr. Judith Mikklossy and Dr. Alan MacDonald approached the role that Borrelia play in Alzheimer’s Dementia from two different perspectives. Dr. Mikklossy looked at the initial disease formation and the effects of Borrelia on Brain-Cell-Cultures, Dr. Alan MacDonald looked at the end process of this infection by observing borrelia in Brain autopsies from Alzheimer’s patients.

I first started becoming seriously ill in 1989 and by the Spring of 1991 I was diagnosed with Multiple Sclerosis. After months of despair at the lack of concern by my physicians, I finally collapsed in the street. I was unable to walk, drive, read a book, or control my body contortions.

I was sent to the neurology ward of the closest hospital St. Luke’s. This hospital employed different neurologists than the clinic where I had been doctoring for two years. I had poorly controlled atrial fibrillation, an enlarged heart, severe pressure in my head, and a visual field where my eyesight was reduced to a fuzzy disk with completely distorted peripheral vision. I was racked with pain, fevers, sweats, and was having both auditory and visual hallucinations.

The doctors were at a loss. What had been considered as Multiple Sclerosis was now an unknown mystery disease.

After a week waiting for answers to various tests, I was put on a waiting list for a nursing home. My doctors gave me nothing but dire news of my prognosis. My personal family doctor and the neurologist I had been seeing were on vacation all week. (This turned out to be a blessing.)

I entered the hospital on a Friday and by Monday I had not seen any take charge doctor. After three days of being bed ridden and given supportive care by well-meaning nurses, the on-duty neurologist that saw me, visited me Monday morning and looked bone tired. This was the first time Dr. Barbara Martyn had ever seen me. (I had been diagnosed at the clinic across town with “MS” for over a year and had seen dozens of doctors and a half dozen specialties at a cost of over $100,00)

This doctor had seen me all of 10 minutes and suggested to me that I did not have MS but rather that I had Lyme disease. She ordered that a 20 day course of intravenous Rocephin be started immediately. But she also continued with the MS tests that had been ordered over the weekend.

I was told there was a long wait to get a brain MRI. Out hospital patients had a four month wait and in-hospital patients had to wait 10 days. Within a few hours of seeing this doctor I had both a CAT-Scan and an MRI.

Dr. Martyn MD (Now deceased from breast cancer) had over the weekend been attending the International Lyme Disease Conference in Arlington Virginia, and only had 4 hours sleep because her flight was delayed. Yet because of that conference she was able to look at my chart and in five minutes decided that Lyme disease was now the most likely cause of my multitude of multi-systemic maladies.

But all of this is a story for another time.

My misdiagnosis with Multiple Sclerosis galvanized my commitment to learn more about the spirochetal disease that was literally swimming inside my brain. As a graduate student 10 years earlier I had worked at the next door specialty hospital and worked with a Tertiary Sphillis patient that had failed three attempts of ever increasing doses of IM Penicillin. So having spirochetes in my brain was not a comforting thought.

Through my association with a Nurse Educator (Barbara Jones RN, MS) it became clear to me in 1991 that other MS patients just like me also had been misdiagnosed and actually had Lyme disease. I felt that what I was experiencing, felt like an infection of my brain, but it also manifested much like dementia.

I could not think clearly. When I spoke I now substituted easy words for hard words, reading black text on white paper gave me seizures, I got lost easily, I was both seeing and hearing things that weren’t real. Emotionally it was like I had a lobotomy that had cut all the feeling out of my brain. I had intellect, but no emotions. Other than uncontrollable urges to cry, I felt as though I had no emotional contact to the world.

That first day of antibiotic therapy, the IV Rocephin caused every muscle in my body to twitch and my body to spasm. The pressure in my head doubled, my entire body perspired and I spiked high fevers. It was this first few hours of agony that I became committed to better understand Lyme disease, and its affects on the human brain. At this time I did not know that my decades of running in the woods and meadows had exposed me to many tick-borne diseases.

As part of my journey I attended every medical conference that I could get to, and by 1997 I had attended well over a dozen conferences, and I tried my best to make sense out of what the CDC and Yale Medical were reporting: It didn’t make any sense?

I kept asking myself “Where are the pathology studies? Why aren’t they looking in the brain.”

I didn’t know then that human pathology studies would never be done with any American tax-payer dollars, and that the CDC and NIH would shoot down all requests for brain-autopsies done in America that would look for spirochetes in the brain.

My first encounter with the CDC hiding information:

I had been a graduate student at the U of MN School of Medicine for two years, and after I was able to walk again. (I didn’t drive much for the next five years) I visited my old mentor at the Medical School to talk to him about this misunderstood disease. Dr. Eugene Cotton was the head of the medical school, and he immediately became enthralled with what I was saying.

I was a Lyme patient who could speak to him in medical terms of what I was going through and explain the odd contradictions that I was encountering with medical experts. Gene immediately spoke up. His friend was the head of the CDC and he had just seen a study by Dr. Judith Miklossy that showed the presence of Borrelia burgdorferi in the brains of 13 consecutive Alzheimer’s patients in Switzerland.

He was so concerned with these findings that he ordered a brain-autopsy study to be done with American dollars, but that the work be done in secret in Canada and no results to be published or reported without going through the CDC.

No results were ever released.

So I called the graduate assistant to the doctor and was met with nothing but hostility and his repeating that all results were proprietary and were never meant to be pubished.

WHAT? We paid for this study! What good is a public health study if the results aren’t shared with the medical community?

Miklossy J, Kasas S, Janzer RC, Ardizzoni F, Van der Loos H. Further ultrastructural evidence that spirochaetes may play a role in the aetiology of Alzheimer’s disease. 1994 Neuroreport. 2;5(10):1201-4.

How research on Lyme is hindered by poor science: It astounded me that all research conducted on animals used only strain B-31 a laboratory strain of Borrelia not found in ticks. More disturbing was that every far-reaching conclusion about diagnosis, and treatment success was based entirely on antibody serology tests created using lab strain B-13.

Over and over repeatedly these antibody tests had been proven unreliable and several published studies pointed out how nebulous these tests were and how flipping a coin was just as accurate. All conclusions about neuroborreliosis were based almost entirely on unreliable antibody-serology tests! Diagnosis was made by serology, and cure was determined by a drop in antibodies. No one at the CDC or major medical institutions seemed to have interest in cracking a few heads open and looking for spirochetes with better tools.

[See photo of testing failures]

The few incidents of culture positives in patient’s after receiving antibiotic treatment, were being purposely ignored and never acknowledged or referenced in papers by the CDC. By 1995 it was clear to me that when it came to the pathology of neuroborreliosis, the Lyme-patient community was completely on their own.

JUST LIKE MEDICAL ADVANCES IN THE 19TH CENTURY, INDIVIDUALS WERE NOW TAKING IT UPON THEMSELVES TO DO THE RESEARCH THAT THE PAID EXPERTS REFUSE TO DO.

In 1994 I had administrated an antibiotic treatment study in Pine County Minnesota for MS patients. I enrolled 26 MS patients diagnosed by both MRI and spinal fluid findings. We only enrolled seronegative patients using either the IGenix Lyme ELISA test or Marshfield Clinic Lyme serology tests. I insisted that only seronegative patients be enrolled and treated. I chose negative patients with clinical symptoms, because these were the patients that were slipping through the cracks in the medical system and not receiving treatment simply because the Lyme antibody tests were inaccurate.

We fell short of our goal of 40+ patients and a big part of that was I felt, the lack of cooperation by the MS Society. Not only could I not speak at their local MS Support Groups to enroll patients, but the MS Support groups would not even distribute our consent forms and brochure. One MS Support Group leader told me that all Lyme disease did was offer false hopes.

Most MS patients were told that Lyme disease had no connection to MS, and in one instance where I spoke to MS patients at the Houghton Michigan MS support group, the MS society flew out a representative one week later for a special meeting with the group, and she spoke very harshly to the support group who had allowed me to speak. Eight members of that group were so outraged that the very next month they splintered off from the MS support network, and formed the first Houghton-Hancock LDSG. After I spoke I arranged for a LLMD near Green Bay WI to treat any and all of the MS patients who could not get treated in Michigan. In all, eight of the MS patients had dramatically improved on antibiotics.

One of those patients enrolled in our LEAMS study (Lyme Endemic Area MS Study) and went from crutches to walking and made cognitive improvements to the point of renegotiating his divorce settlement and getting total custody of his kids. He even appeared on a local talk show and encouraged other MS patients to get treated with antibiotics. The backlash by the Upper Peninsula Health Department was swift and completely unyielding in their opinion that treating Lyme disease long-term or treating MS with antibiotics was a waste of time and dangerous.

Of the 26 MS patients in our antibiotic trial, only three seroconverted and had positive serologic evidence of having Lyme disease. But a total of 8 of the 26 patients overall responded favorably to three months of antibiotics. Unfortunately, 17 of 26 did not respond at all.

After a one year follow-up, we discovered that one patient in our treatment failure group had stayed on amoxicillin for 15 months and made a nearly total recovery.

What I concluded from our MS antibiotic treatment study was this:

  • # of Patients Conclusion Length of Rx w/Amox/doxy/Biaxin
  • 3 Had Lyme disease and made partial recoveries 3 months
  • 5 5 patients had improvement but were not seropositive 3 months
  • 17 Had no response to antibiotics either doxy/amox/or Biaxin 3-months Rx
  • 1 One MS patient had 15 months of amoxicillin and made a near full recovery

I found the results disappointing and had hoped for better. My thoughts on our results are: Not all MS is caused by the Lyme bacteria, and that our treatment length was far too short. It would be years later in 2004 when Alan MacDonald would discover an association in MS with nematode parasites and that these parasites were often associated with Borrelia and found in the human brain in many dementia cases.

It may well be that as many as half the cases of MS and dementia are caused by mixed infections. Also we knew nothing of other Borrelia species like Borrelia myamotoi that also enters the brain, and is seronegative on lyme tests.

I was very frustrated. Our study was ignored by the Minnesota health department and they would not even consider a study of their own. When I presented my proposal to State Representative Mary Murphy, Dr. Michael Osterholm PhD the state epidemiologist crashed the meeting insisting that he talk with her alone. (She got very angry.) Osterholm said it was ridiculous to even report MS in surveillance reports because it wasn’t an infectious disease.

He also repeatedly said that hunters cannot get Lyme disease in the Fall because the female ticks won’t feed on humans in those months??? He made these comments because I had helped pass a bill to distribute Lyme information to hunters. Of course he lied.His own paper that he gave Representative Murphy stated that Lyme disease can be contracted in any month of the year and cases had been reported in all months in Minnesota.

It was clear that the State Health department wasn’t going to be any help in a human pathology Lyme Study. It was now 1995 and I had run out of medical sources to get for better answers and better studies? But this was the year that I met Dr. Alan MacDonald.

I first met Dr. Alan MacDonald (pathologist) at an LDF conference. Between talks he was carrying a small boy on his shoulders and he joyfully talked about creating a CD-ROM of various forms of spirochetes and pontificated about the role of variant forms. Almost simultaneously we remarked on the extraordinary work by Dr. Gabriel Steiner in Germany and his findings of “crescent-like” forms in the brains of MS patients.

As luck would have it Dr. Vincent Marshall the expert on Gabriel Steiner was at this conference and his insights on spirochetes in the human brain in MS patients were invaluable to me.

No one else in America had been looking back 75 years in the European Literature for a spirochete connection to MS. While it is easy to dismiss any one published study on MS and spirochetes, it is complete denial to dismiss over 30 pre-WWII published studies by a dozen different researchers in four different countries.

I knew when I met Alan and Vincent that I had found researchers who had the same mindset and goals as me.

In late 1996 we discussed doing brain autopsies on actual patients. It was a patient in our LDSG that led us to our our first candidate. This patient was from a very endemic area of Wisconsin, and he too was all about finding answers through better science.

Jim’s father was a lifelong farmer, hunter and outdoorsman. Unfortunately this vibrant active man was now wasting away in a nursing home, he had dementia later confirmed by autopsy and the presence of amyloid plaques as Alzheimer’s disease. In addition to dementia this patient also had about a dozen symptoms of Lyme disease. More importantly he had two sons with Lyme disease that had been misdiagnosed with rheumatoid arthritis and MS who both recovered on long-term antibiotics (two years). The brothers both recovered on antibiotics and were now asking if their dying father could also have Lyme disease? And more to the point: did Lyme disease cause his dementia?

Jim Forris from Ashland WI battled with his family to do this autopsy. Like most families they just wanted this dark chapter in their lives to be closed and doing an autopsy was a lot of work, it was expensive, the process seemed morbid, and what guarantee was there that he would have spirochetes in his failing brain?

But Jim had the power of attorney over his father’s affairs, and without any more consultation he had his father’s brain harvested at death, and then shipped it to New York to Dr. Alan MacDonald.

The results were beyond our expectations. Jim’s father had Borrelia burgdorferi in every cross section of his brain. More importantly in 1997 Dr. MacDonald was the first to capture Borrelia intracellular inside neurons and had serial sections showing the spirochete could transit brain cells with apparent ease. Spirochetes were found attached to glial cells and many were seen in extracellular spaces.

Unfortunately at this time it was not even a consideration to stain for amyloid and Borrelia on the same slide. Alan would do this a decade later with spectacular results!

In medicine this should have been a huge deal.A major discovery. But inexplicably it was completely ignored. We even kept the stored unstained paraffin blocks available to the patient’s doctors and others to see for them selves. No one was willing to test the tissues for themselves.

When Jim approached his father’s doctors with the offer to share the formalin fixed brain with them for their own research, their response to Jim Forris’s sincere and generous offer was to get a restraining order. A restraining order! This was no longer just denial or ignorance, this was now obfuscation and obstruction of medical science. In medicine not only can ignorance be bliss, but it can also be used as plausible deniability.

Once it was determined that this dementia patient actually had Lyme disease and they had repeatedly denied even testing for Lyme: The response was that the clinic in Duluth MN wanted nothing more to do with this case or the family of the patient. All discussions were squashed!

These images below should have been regarded as a medical breakthrough just as important as finding the cause of Legionaire’s disease or the true cause of ulcers by H. pylori. Instead like all great finds in Lyme disease research, it was either ignored or met with disdain.

Intracellular Borrelia inside brain neurons and glial cells explained a lot about what we had been seeing in patients.

• Neuro Lyme patients often had severe neurologic symptoms
• Few bacteria were ever seen in the blood
• Blood tests were often negative due to low infection load in blood
• Patients often relapsed after recommended lengths of antibiotics
• Treatments required higher dose of antibiotics, that are dosed longer and often in combinations to reach therapeutic/bactericidal levels in the brain

We were excited at this finding, but had no idea of how much more convoluted the pathology would become. It became clear we had to better understand the interactions of Borrelia with brain cells.

We were elated when in 2006 the CDC funded study by doctors Jill Livengoode and Dr. Robert Gilmore. They confirmed our finding of Borrelia having the ability to penetrate both glial cells and human neurons. But inexplicably the very study that the CDC funded was almost immediately suppressed by the CDC, and several administrators even disparaged their work as though to contradict their findings by saying: “…this was a test tube study and means nothing.”

Neither Gilmore or Livengoode appear to be speaking openly about their collaboration? And to my knowledge do not publically make comments about its importance. A similar situation appears to be happening in Canada where researchers have photographed live Borrelia swimming through blood vessels with ease. What is going on?
What is the ultimate agenda with these denialists? It certainly isn’t science or they would fund a multi-national brain autopsy study to deny or confirm Alan’s and Livengoode’s work on intracellular penetration in-vivo.

Microbes Infect. 2006 Nov-Dec;8(14-15):2832-40. Epub 2006 Sep 22.

Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.

Livengood JA, Gilmore RD Jr.
Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA.

So now with the CDC all but denying the existence of Livengoode and Gilmore’s work things looked even more bleak in the world of lyme disease pathology research.

=========================================

Enter Dr. Judith Mikklossy

Where my quest led me was to attend every science based Lyme conference that Tom Forschner and Karen Forschner of the LDF planned and administrated. (I believe the Lyme Disease Foundation conferences were for over a decade the most medically sound, research based Lyme conferences I ever attended.)

It was in 1997 when I first met Dr. Judith Miklossy a Neuro-Pathologist who had been researching dementia for several years. Judith presented her Swiss study of brain-autopsies on 13 Alzheimer’s patients. All 13 had spirochetes and her aged matched controls (no dementia) were negative for Borrelia.

Judith even isolated live bacteria from one of the subjects. This would lead to several more studies including using that isolate to measure the effects on rat-brain cultures. Dr. Mikklossy continues to focus on Borrelia and its role in causing dementia, and its prevalence in Alzheimer’s brains.

https://jneuroinflammation.biomedcentral.com/…/1742-2094-8-…

But there was another pathologist presenting at the same conference and he also had been working with the idea that Borrelia was playing a role on the pathology of Alzheimer’s Dementia. His name was Dr. Alan MacDonald MD, and he had a keen interest in not only the spiral form, but also the spherical forms of Borrelia, and felt they had a role in the pathogenesis of dementia.

MacDonald AB: Borrelia in the brains of patients dying with dementia. JAMA. 1986, 256: 2195-2196.

While Judith was concentrating on the mechanism of pathogenesis by looking at Rat-Brain model, Alan’s method was to work backwards: Alan chose to look at hundreds of brain sections from hundreds of Alzheimer’s patients, and to look at what the end process of neuroborreliosis looks like, and to attempt to explain the mecahnisms of changes seen in the Alzheimer’s brain.

When we combine Mikklossy’s work and Alan MacDonald’s work, we see that they meet in the middle reaching similar conclusions and findings.

McGeer PL, Itagaki S, Tago H, McGeer EG: Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR. Neurosci Lett. 1987, 79: 195-200. 10.1016/0304-3940(87)90696-3.

Mikklossy

Dr. Judith Mikklossy investigated how Borrelia interacts with specific brain cells, and developed what for all intents is a petri dish model of Alzheimer’s disease. All the markers we look to see in Alzheimer’s brain is found withing mere weeks of adding Borrelia burgdorferi to rat brain cultures.

With the addition and enrichment with brain-microglia cells, the various cells immediately produced its first marker: precursor amyloid protein.

These are the other markers she observed in just eight weeks.

1 Precursor Amyloid Protein APP production
2 Cleavage of APP to Beta Amyloid
3 Conversion to Beta sheet amyloid
4 Hyperphosphoralation of microtubule protein Tau
5 Neurofibrillary tangles
6 Vacuole-like spaces

Everything we expect to see in an Alzheimer’s brain was seen except true plaques.

MacDonald

Alan took a different approach to Alzheimer’s research and the role of spirochetes.

Registering more living patients for brain autopsies is an extremely slow process with poor success rate because family members will often go against the patient’s wishes and at the last minute will cancel the tissue harvest. Also the process is expensive without an institution with the equipment and funding to do the work.

Here is what is involved with registering patients for a brain autopsy:

• A family discussion and agreement to pursue pathology research
• Legal consent forms must be signed
• Costs per brain are $1,000-5,000 depending on what is done
• A large enough patient sample across many states is needed to be statistically relevant.
• Expert techniques are needed in: sectioning, staining, and fluorescent microscopy using individually designed DNA probes
• Storage of samples
• Data analysis

As a way to speed up the process and reduce costs and legal concerns, Alan ordered brain samples (both frozen and paraffin blocks) from Alzheimer’s Brain Banks like Harvard.

Alan sectioned and stained hundreds of samples and found some amazing things that I have listed below.

Borrelia often forms biofilms within the human Alzheimer’s brain
• More than one species of Borrelia is involved
• The spirochetes either attract amyloid or helps produce it as the bacteria biofilms are found interspersed inside the amyloid plaques
• Nematode worms are sometimes seen in the diseased brain of both MS and Alzheimer’s patients
• The nematode gut stains positive by DNA probes for Borrelia
• The nematodes destroy brain tissue and deposits feces and eggs in the brain
Borrelia biofilms are seen in fatal glioblastoma tumors
• Both Borrelia burgdorferi and Borrelia mayonii have been found within the testicle of one patient
• In severe dementia, amyloid can sometimes be detected in the blood using amyloid stains, this might be a blood test for Alzheimer’s?

So while Dr Mikklossy looks for the genesis of Alzheimer’s disease, Alan MacDonald looks at the end state of the disease process and asks what the role Borrelia play?

They have reached similar conclusions:

Borrelia can form “colonies or biofilms” in the brain.
Borrelia can penetrate blood vessels and weaken blood vessels possibly leading to strokes
Borrelia bacteria have a tropism (attraction) for the brain and for specific brain cells.
Borrelia is found both intracellular and extracellular in the brain
• While the bacteria is detected in the brain by autopsy, the blood can remain negative for the associated antibodies
• The blood-brain-barrier represents a therapeutic challenge to treat effectively and maybe considered a treatable but incurable condition
Borrelia may well be part of the biochemical process that leads to amyloid production
• The debate over whether Borrelia like Syphilis can cause dementia is now overwhelmingly supportive of a new category of dementia: “Borrelia Associated Dementia”

END PART ONE

https://jneuroinflammation.biomedcentral.com/…/1742-2094-8-…

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MacDonald, Alan in European Journal of Clinical Microbiology 32(8) · March 2013 with 32 Reads

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For More:

What Makes the Bacteria Behind Lyme Disease Tick?

http://www.infectioncontroltoday.com/bacterial/what-makes-bacteria-behind-lyme-disease-tick?  Feb, 2018

Ashley Groshong

UConn Health researchers led by postdoctoral fellow Ashley Groshong, shown here in UConn Health’s Spirochete Research Lab, are advancing understanding of how the bacteria Borrelia burgdorferi transmits Lyme disease, pointing to the potential for ultimately developing therapeutics to target this system. Courtesy of UConn Office of the Vice President for Research

What Makes the Bacteria Behind Lyme Disease Tick?

Researchers from UConn Health are advancing the understanding of how the causative bacterial agent of Lyme disease, Borrelia burgdorferi (Bb), survives in ticks and mammals.

Connecticut residents are all too familiar with Lyme disease, but the precise mechanisms of how humans become infected are still unclear. Researchers from UConn Health are advancing the understanding of how the causative bacterial agent of Lyme disease, Borrelia burgdorferi (Bb), survives in ticks and mammals.

The findings from Ashley Groshong, a postdoctoral fellow in the Spirochete Research Lab at UConn Health, and her colleagues were recently published in mBio.

Here’s a refresher on the typical steps involved in the spreading of Lyme disease.

An infected black-legged tick (Ixodes scapularis) feeds on and infects a mammal, like a white-footed mouse, to transmit a pathogen (i.e. Borrelia burgdorferi) to its next mammalian host. While the tick may prefer to feed from small rodents or deer, oftentimes humans are an accidental host. In this case, transmission of the bacteria to humans results in disease pathology.

This bacterial pathogen is a spirochete, which means it has a unique spiral shape, and it is slow to replicate. It also depends entirely on its host for nutrients, a unique characteristic that has drawn attention from many Lyme researchers. While previous genetic analyses have suggested that the Bb’s genome encodes a cellular transport system capable of importing nutrients from the host in the form of peptides, the importance of the system for viability and pathogenesis had never been established.

“We wanted to target the energy domain of the system to understand exactly how important this system is for survival and proliferation during infection,” explains Groshong. “If we understand how B. burgdorferi acquires its nutrients from its hosts and which nutrients are essential, it could potentially lead to a novel target for therapeutic intervention.”

The peptide transport system is quite complex, preventing previous evaluation of its role in the bacteria. To better understand the importance of peptides, a source of amino acids, Groshong and the UConn Health team adopted a novel approach. Groshong created a mutant version of B. burgdorferi that effectively blocks the spirochete’s normal methods of consuming peptides by targeting the lynchpin of the transporter, the part of the system that provides energy for peptide transport.

The research showed that spirochetes deprived of peptides failed to replicate, which indicates that peptide uptake is essential for bacterial viability and ability to infect. In other words, Groshong and the UConn Health team have shown that if Bb’s transport system is inhibited, it would be possible to block the proliferation of the bacteria in an infected mammal, such as a human or rodent. Interestingly, this is the only pathogen demonstrated to require peptides for basic viability, making this a unique find in the world of pathogenic bacteria.

Lyme disease research is particularly important for Connecticut residents, where the condition was first recognized in Lyme, Conn., in 1975. According to the Connecticut State Department of Public Health, approximately 30,000 people in the state are diagnosed with Lyme disease each year.

“When it comes to helping Connecticut tackle Lyme disease, UConn is providing support on all fronts,” says Radenka Maric, vice president for research at UConn and UConn Health, “from tick testing at the Connecticut Veterinary Medical Diagnostic Laboratory to innovative research like Dr. Groshong’s at the Spirochete Research Lab. UConn’s faculty, postdoctoral fellows, and students are conducting research to find solutions to the major health challenges we face today.”

Groshong plans to build on this research through a project that will explore possible ways to target this system for the development of therapeutics and to evaluate if a limited peptide environment, such as the mammal, promotes the formation of antibiotic-tolerant persister cells. This research will be funded through a Blackman Fellowship from the Global Lyme Alliance.

According to Groshong, there is still a long way to go before this research could translate into a new treatment option, but she’s hopeful about what this discovery means for the study of Lyme disease.

“Right now, our options for treating and preventing this infection are limited and not specific to the bacteria,” says Groshong. “Our goal is to conduct research that could lead to better understanding of how these bacteria cause disease, as well as novel and targeted approaches to new therapies.”

Other UConn Health authors include Abhishek Dey, Irina Bezsonova, Melissa J. Caimano, and Justin D. Radolf.

Source: UConn Health

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**Comment**

This research presents patients with some definite hope for novel treatment.

One word; however, about the elephant in the room that needs to be addressed.  Researchers keep saying that the way to acquire Bb is through a black-legged tick.

Period.  End of story.

What about other ticks, other insects?  What about sexual transmission, congenital transmission & via breast milk?  What about through bodily fluids? There is evidence for all of these modes of transmission yet…..

the elephant keeps standing, unnoticed in the middle of the room.

People would rather blame “climate change,” to obtain hefty grants to provide them with monetary support for the next few years rather than truly help sick and dying patients who need these questions answered.  These are practical questions that affect our day to day decisions as humans.

According tick expert, John Scott, who has volunteered some 30,000-plus hours as a citizen scientist and was awarded a Sovereign’s Medal for Volunteers in recognition of 27 years of research and advocacy on Lyme disease and tick populations in Canada,

Climate change has nothing to do with tick movement. Blacklegged ticks are ecoadaptive, and tolerate wide temperature fluctuations. On hot summer days, these ticks descend into the cool, moist leaf litter and rehydrate. In winter, they descend into the leaf litter, and are comfortable under an insulating blanket of snow. Ticks have antifreeze-like compounds in their bodies, and can tolerate a wide range of temperatures. For instance, at Kenora, Ontario, the air temperature peaks at 36°C and dips to –44°C, and blacklegged ticks survive successfully……ticks are marvellous eco-adaptors. They will be the last species on the planet.” https://madisonarealymesupportgroup.com/2017/08/14/canadian-tick-expert-climate-change-is-not-behind-lyme-disease/

He also states:

Any research on ticks and climate change is inconclusive––in essence, there is no validity. The long-range, futuristic projections and statistical models are bogus science because blacklegged ticks have already been found in northern Canada. In fact, we documented blacklegged ticks on migratory songbirds in northern Alberta dating back to 1998. Any allocation of government funding for ticks and climate change research is a complete waste of taxpayers’ money. It will not help Lyme disease patients one iota.https://madisonarealymesupportgroup.com/2017/08/14/canadian-tick-expert-climate-change-is-not-behind-lyme-disease/

Will someone please address the elephant?