Archive for the ‘Parasites’ Category

Panel Says TBI’s Have Reached Epidemic Levels

https://m.medicalxpress.com/news/2018-04-tick-borne-diseases-epidemic-panel.html

Tick-borne diseases reach epidemic levels, panel says

April 16, 2018
by Delthia Ricks, Newsday
Lyme disease
Adult deer tick, Ixodes scapularis. Credit: Scott Bauer/public domain

Tick-borne infections have reached epidemic proportions on Long Island, where children are disproportionately affected by Lyme disease and other infections transmitted by the eight-legged creatures, a panel of top scientists announced recently.

“Lyme disease is mostly a disease of children and curiously mostly a disease of boys,” Jorge Benach said at a recent symposium at Stony Brook University School of Medicine. Benach, who discovered the bacterium that causes Lyme disease, is a molecular geneticist at Stony Brook University School of Medicine.

His observation that Lyme disease is mostly an  of children was corroborated by Dr. Christy Beneri, a pediatrician at Stony Brook Children’s Hospital. She said her institution encountered a wide range of tick-borne illnesses annually and that boys tended to outnumber girls in the number of infections. The most likely reason for the disparity, Beneri said, is the tendency among boys to play outdoors in wooded areas where ticks thrive.

In the extensive pediatric research Beneri presented at the symposium was evidence of some children developing Bell’s palsy, a temporary facial paralysis that occurs when the Lyme bacterium affects a cranial nerve. The paralysis resolves with antibiotic treatment, Beneri said.

Beyond the Lyme bacterium, ticks on Long Island have been found to harbor babesia and anaplasma.

Babesia are protozoa, or parasitic, infectious agents that hone in on red blood cells, similar to the way a malaria parasite invades the same cells.

Anaplasmosis is an infection caused by the bacterium Anaplasma phagocytophilum. It can trigger aches, fever, chills and confusion.

Beneri and Benach were among five leading Stony Brook experts, including university president Dr. Samuel Stanley, who addressed what they described as a mounting epidemic of infections caused by the ever-expanding range of ticks. Stanley, who was the first speaker, is a specialist in infectious diseases.

“New York bears a disproportionate impact from tick-borne diseases,” Stanley said at the symposium, which was held in a lecture hall in the university’s health sciences building. “This is a regional and state problem.”

New York has the highest number of confirmed Lyme  cases nationwide, according to the U.S. Centers for Disease Control and Prevention, which has cataloged more than 95,000 Lyme infections in the state since 1986. Suffolk County has long been ground zero for the ailment on Long Island, studies consistently have shown.

“Cases in Suffolk County hover between 500 and 700 and this is just for the reported cases,” Benach said, noting that Suffolk has among the highest rates of many tick-transmitted infections because of the dense infiltration of the insects in county.

Typical Lyme symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans, said Dr. Luis Marcos, a specialist in internal medicine and infectious diseases.

Marcos presented data showing the wide range of illnesses caused by ticks throughout the region, including Borrelia miyamotoi, a corkscrew-shaped bacterium identified in recent years as the cause of a relapsing fever.

Dr. Eric Spitzer, a pathologist, discussed the many laboratory tests that Stony Brook used to arrive at a diagnosis of a tick-transmitted illness. He said that for years, doctors nationwide sent specimens to the university for analysis because of its well-known precision. Testing of those specimens earned the university $32 million over a 20-year period, he said.

Panelists identified the most prevalent ticks on Long Island as the American dog tick; the invasive lone star tick, which migrated from Southern states; and the blacklegged tick, known as deer tick.

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For more:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/

https://madisonarealymesupportgroup.com/2016/03/08/anaplasmosis/

http://danielcameronmd.com/best-antibiotics-treat-borrelia-miyamotoi/ The study authors demonstrated that B. miyamotoi is susceptible to doxycycline, azithromycin, and ceftriaxone but resistant to amoxicillin in vitro. The next step would be to show whether these drugs work in patients.

 

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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-…

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

MacDonald AB, Miranda JM: Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987, 18: 759-761. 10.1016/S0046-8177(87)80252-6
MacDonald AB: Concurrent neocortical borreliosis and Alzheimer’s Disease. Ann N Y Acad Sci. 1988, 539: 468-470. 10.1111/j.1749-6632.1988.tb31909.x.
Pappolla MA, Omar R, Saran B, Andorn A, Suarez M, Pavia C, Weinstein A, Shank D, Davis K, Burgdorfer W: Concurrent neuroborreliosis and Alzheimer’s disease: analysis of the evidence. Hum Pathol. 1989, 20: 753-757. 10.1016/0046-8177(89)90068-3.

Miklossy J, Kuntzer T, Bogousslavsky J, Regli F, Janzer RC: Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis. Acta Neuropathol. 1990, 80: 568-572. 10.1007/BF00294622.

Miklossy J: Alzheimer’s disease – A spirochetosis?. Neuroreport. 1993, 4: 841-848. 10.1097/00001756-199307000-00002.

Baker HF, Ridley RM, Duchen LW, Crow TJ, Bruton CJ: Evidence for the experimental transmission of cerebral beta-amyloidosis to primates. Int J Exp Pathol. 1993, 74: 441-454.

Baker HF, Ridley RM, Duchen LW, Crow TJ, Bruton CJ: Experimental induction of beta-amyloid plaques and cerebral angiopathy in primates. Ann N Y Acad Sci. 1993, 695: 228-231. 10.1111/j.1749-6632.1993.tb23057.x.

Baker HF, Ridley RM, Duchen LW, Crow TJ, Bruton CJ: Induction of beta (A4)-amyloid in primates by injection of Alzheimer’s disease brain homogenate. Comparison with transmission of spongiform encephalopathy. Mol Neurobiol. 1994, 8: 25-39. 10.1007/BF02778005.

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

Alzheimer’s disease Braak Stage progressions: Reexamined and redefined as Borrelia infection transmission through neural circuits Medical Hypotheses 68(5):1059-64 · February 2007
Alzheimer’s neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochete in Medical Hypotheses 68(4):822-5 · February 2007 with
MacDonald, Alan Alzheimer’s & dementia: the journal of the Alzheimer’s Association 2(3) · July 2006

Spirochetal cyst forms in neurodegenerative disorders,… hiding in plain sightArticle in Medical Hypotheses 67(4):819-32 · February 2006
Gestational Lyme borreliosis. Implications for the fetusArticle · Literature Review in Rheumatic Disease Clinics of North America15(4):657-77 · December 1989
Miklossy J, Kasas S, Janzer RC, Ardizzoni F, Van der Loos H: Further morphological evidence for a spirochetal etiology of Alzheimer’s Disease. NeuroReport. 1994, 5: 1201-1204.
Schaeffer S, Le Doze F, De la Sayette V, Bertran F, Viader F: Dementia in Lyme disease. Presse Med. 1994, 123: 861
Fallon BA, Nields JA: Lyme disease: a neuropsychiatric illness. Am J Psychiatry. 1994, 151: 1571-1583.
Miklossy J: The spirochetal etiology of Alzheimer’s disease: A putative therapeutic approach. Alzheimer Disease: Therapeutic Strategies. Proceedings of the Third International Springfield Alzheimer Symposium. Edited by: Giacobini E, Becker R. 1994, Birkhauser Boston Inc., 41-48. Part I
Miklossy J, Gern L, Darekar P, Janzer RC, Van der, Loos H: Senile plaques, neurofibrillary tangles and neuropil threads contain DNA?. J Spirochetal and Tick-borne Dis (JSTD). 1995, 2: 1-5.
Miklossy J, Darekar P, Gern L, Janzer RC, Bosman FT: Bacterial peptidoglycan in neuritic plaques in Alzheimer’s disease. Azheimer’s Res. 1996, 2: 95-100.
Miklossy J: Chronic inflammation and amyloidogenesis in Alzheimer’s disease: Putative role of bacterial peptidoglycan, a potent inflammatory and amyloidogenic factor. Alzheimer’s Rev. 1998, 3: 45-51.
Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ: Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis and may be associated with Alzheimer disease. J Alzheimer’s Dis. 2004, 6: 1-11.
Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K: Beta-amyloid deposition and Alzheimer’s type changes induced by Borrelia spirochetes. Neurobiol Aging. 2006, 27: 228-236. 10.1016/j.neurobiolaging.2005.01.018.

Miller LM, Wang Q, Telivala TP, Smith RJ, Lanzirotti A, Miklossy J: Synchrotron-based infrared and X-ray imaging shows focalized accumulation of Cu and Zn co-localized with beta-amyloid deposits in Alzheimer’s disease. J Struct Biol. 2006, 155: 30-37. 10.1016/j.jsb.2005.09.004.

MacDonald AB: Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete. Med Hypotheses. 2006, 67: 592-600. 10.1016/j.mehy.2006.02.035.

Larsen P, Nielsen JL, Dueholm MS, Wetzel R, Otzen D, Nielsen PH: Amyloid adhesins are abundant in natural biofilms. Environ Microbiol. 2007, 9: 3077-3090. 10.1111/j.1462-2920.2007.01418.x.

Meer-Scherrer L, Chang Loa C, Adelson ME, Mordechai E, Lobrinus JA, Fallon BA, Tilton RC: Lyme disease associated with Alzheimer’s disease. Curr Microbiol. 2006, 52: 330-332. 10.1007/s00284-005-0454-7.
Miklossy J: Chronic inflammation and amyloidogenesis in Alzheimer’s disease – role of spirochetes. J Alzheimer’s Dis. 2008, 13: 381-391.

Honjo K, van Reekum R, Verhoeff NP: Alzheimer’s disease and infection: do infectious agents contribute to progression of Alzheimer’s disease?. Alzheimers Dement. 2009, 5: 348-360. 10.1016/j.jalz.2008.12.001.
Loeb MB, Molloy DW, Smieja M, Standish T, Goldsmith CH, Mahony J, Smith S, Borrie M, Decoteau E, Davidson W, McDougall A, Gnarpe J, O’DONNell M, Chernesky M: A randomized, controlled trial of doxycycline and rifampin for patients with Alzheimer’s disease. J Am Geriatr Soc. 2004, 52: 381-387. 10.1111/j.1532-5415.2004.52109.x.PubMedGoogle Scholar
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Kim HS, Suh YH: Minocycline and neurodegenerative diseases. Behav Brain Res. 2009, 196: 168-179. 10.1016/j.bbr.2008.09.040.
Miklossy J, Kasas S, Zurn AD, McCall S, Yu S, McGeer PL: Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis. J Neuroinflammation. 2008, 5: 40-10.1186/1742-2094-5-40.

McGeer PL, McGeer EG: Local neuroinflammation and the progression of Alzheimer’s disease. J Neurovirol. 2002, 8: 529-538. 10.1080/13550280290100969.

Guo JP, Arai T, Miklossy J, McGeer PL: Abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer disease. Proc Natl Acad Sci USA. 2006, 103: 1953-1938. 10.1073/pnas.0509386103.

Miklossy J, Rosemberg S, McGeer PL: Beta amyloid deposition in the atrophic form of general paresis. Alzheimer’s Disease: New advances. Proceedings of the 10th International Congress on Alzheimer’s Disease (ICAD). Edited by: Iqbal K, Winblad B, Avila J. 2006, Medimond, International Proceedings, 429-433.

Miklossy J: Biology and neuropathology of dementia in syphilis and Lyme disease. Dementias. Edited by: Duyckaerts C, Litvan I. 2008, Edinburgh, London, New York, Oxford, Philadelphia, St-Louis, Toronto, Sydney: Elsevier, 825-844. Series Editor Aminoff MJ, Boller F, Schwab DS: Handbook of Clinical Neurology vol. 89

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For More:

How Proteolytic Enzymes May Help Lyme/MSIDS

Approx. 15 Min.

Systemic Proteolytic Enzymes–What works, What Doesn’t and Why

Written by: Jon Barron  https://jonbarron.org/article/proteolytic-enzyme-formula

Proteolytic enzyme supplements, or systemic enzymes, work to clean out the blood, optimize blood flow, control inflammation throughout the body, as well as repair and rebuild the cardiovascular system.  Although they may have some cancer protective benefits–and there are indeed cancer therapies based on proteolytic enzymes, not to mention a number of studies that support those therapies–the primary benefits we’re looking for when taking systemic, proteolytic enzymes center around their ability to:

  • Control inflammation throughout the body, not just in your joints.
  • Repair and rebuild the cardiovascular system.
  • Optimize blood flow & cleanses blood of debris
  • Prevent and dissolve blood clots by dissolving fibrin
  • Dissolve plaque in your arteries and dental plaque in your mouth.
  • Clean up your immune system.
  • Minimize the impact of allergies but breaking down and removing circulating immune complexes.
  • Improve the ability to exercise and speed up recovery times.
  • Kill bacteria, viruses, and other pathogens.
  • Accelerate recovery from sprains, strains, fractures, bruises & surgery
  • Help with arthritis
  • Help with detoxification
  • Improve body alkalinity
  • Help with sinusitis and asthma
  • Help reduce MS symptoms

And all of these benefits stem from one simple ability: proteolytic enzymes facilitate the breakdown of rogue proteins in your bloodstream and in the soft tissues of your body. In this video, we’re going to take a look at exactly what systemic, proteolytic enzymes are, what they do, how they do it, and what the ideal proteolytic formula looks like.

More info: https://jonbarron.org/article/proteol…

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**Comment** 

Great info here.  At 2:26 he discusses how these enzymes break down protein bonds in invading viruses as well as have the ability to digest and destroy the protein based defense shield of each and every pathogen, allergen, and rogue cell, leading to their elimination.

Can you see how this would help Lyme/MSIDS patients?

Not to mention the foreign protein invaders from the food we eat.  Many Lyme/MSIDS patients have food sensitivities and Mast Cell disorders that if not addressed will cause many symptoms that look identical to Tick borne illness (TBI).  This is why some patients do not improve after taking sufficient antimicrobials.  Antimicrobials will not fix this.

At 6:55 he discusses how research has shown systemic enzymes support healthy blood viscosity and blood platelet aggregation.  Since many TBI’s infect the blood cells of our body, this assistance is extremely helpful.  Parasitemia can cause hyper coagulation, and things like blood thinners help some patients just as much as antibiotics.  Speaking of blood thinners, nattokinase’s ability to balance the clotting ability of the blood is as good as Warfarin’s but without the side effects.  Research has shown it reduces blood pressure as well.  It also dissolves amyloid fibrils, which means it very well may help with Alzheimer’s, and most Lyme/MSIDS patients understand the connection there.

At 7:30 he mentions that papain has been shown to be as effective as the pharmaceutical drugs Butadion and Indomethacin as an anti-inflammatory and that it is even used for treating parasitic worms, another common MSIDS issue.

Talk over Systemic Enzymes with your doctor.  It may very well be the thing that helps you turn the corner in your journey.

For more on Systemic Enzymes:  https://madisonarealymesupportgroup.com/2016/04/22/systemic-enzymes/

Generating 1st Transgenic Ticks to Help Fight Tick-borne Diseases

https://www.unr.edu/nevada-today/news/2018/cabnr-lab-generates-transgenic-ticks

2/21/2018 | By: Robyn Feinberg

Generating first-ever transgenic ticks to help fight tick-borne diseases

College of Agriculture, Biotechnology, and Natural Resources lab receives grant from National Institute of Health for tick research
Tick1180x560Unfed and blood fed larvae, an example of the ticks used in Gulia-Nuss’ lab that demonstrate the differences between an unfed and blood fed larvae. Photo taken by Andrew Nuss, assistant professor at the University of Nevada, Reno.

For those who are active hikers, or find themselves outdoors often, the reality of a tick bite is not unusual, nor are its potential consequences. Ticks are known for transmitting many diseases in animals and humans, especially the deer tick, which is a known carrier of diseases such as Lyme disease, babesiosis, and anaplasmosis.

Monika Gulia-Nuss, assistant professor in the Department of Biochemistry and Molecular Biology at the University of Nevada, Reno, is working on generating transgenic ticks in her lab, the first of their kind, in order to explore new targets for vector control. Vector control is any strategic method used to limit organisms that spread disease pathogens.Monika Gulia-Nuss in her lab

Gulia-Nuss’ lab works specifically on the deer tick and has received a $407,000 grant from the National Institute of Health to continue studies.

“Our focus is to be able to manipulate these ticks in the lab so that we can understand the functions of different genes,” Gulia-Nuss said. “This way we can have a better approach for finding new vaccine, drug or insecticide targets.”

“This particular project that we just got awarded from the National Institute of Health is to develop methods for generating transgenic ticks for functional studies,” Gulia-Nuss said.

Transgenic in this sense means deleting or over-expressing a gene in an organism – in this case the tick. Generating transgenic ticks will not only help the Gulia-Nuss lab explore new areas of vector control, but also help in understanding genes involved in tick-pathogen interactions.

“One of the major impediments in tick research is that we do not have any genetic tools to dissect out the functions of their genes,” Gulia-Nuss said.

The lab knows the functions of certain genes in other organisms, but those specific tools are not readily available when studying ticks, so Gulia-Nuss and her team are building tools.

Originally a mosquito biologist, Gulia-Nuss moved into tick research with little experience with the bloodsucking arachnids. Studying ticks has previously proven difficult for many labs and researchers in terms of time.

“I didn’t know that the tick life cycle is two years,” Gulia-Nuss said. “That was a surprise for me, because with mosquitoes, I was used to 10 days of life cycle, and here I had this organism that takes two years, which is another impediment in tick research.”

Gulia-Nuss’ first move in her transgenic research was to shorten the life cycle of the ticks she was working on.

“When I set up my lab here at the University in 2016, my first goal was to cut the life cycle short to a more manageable time,” she said. “We were able to bring it down to five months from two years, which was a big step forward for us.”

The lab was able to do this by placing the ticks in an incubator set to a higher temperature, increasing their metabolism and therefore causing them to molt faster.

The second step for Gulia-Nuss was to inject tick embryos, something that no one else had ever done before.

“We didn’t even know what manipulation we needed to inject embryos,” Gulia-Nuss said.

Gulia-Nuss’ collaborator and the co-investigator on this grant, Robert Harrell, is an expert in transgenic insects and manages the Insect Transformation Facility at the University of Maryland. Together, they used their expertise in mosquito embryo injections and translated it into the tick research.

“We were able to inject tick embryos, so the shortened life cycle and our ability to demonstrate that we could inject tick embryos were the two main steps that really helped us get this grant,” Gulia-Nuss said.

The hypothesis behind the work

The major hypothesis behind the lab’s research lies in disrupting insulin signaling in ticks so as to affect parasite development.

“If we disrupt insulin signaling in ticks, that will influence their physiology and their behavior, and potentially the development of the pathogen they carry,” Gulia-Nuss said.

Insulin signaling is extremely important for nutrient metabolism, which is in turn, important for all organisms including ticks.

“Nutrients are important for a parasite developing inside an organism because the parasite requires all of their nutrients from the host,” Gulia-Nuss said. “To get those nutrients, the insulin signaling of the host should be in perfect order, but if we disturb the insulin signaling in the host, that might affect parasite development.

The lab is planning to use a technology called CRISPR-Cas9, which has the ability to manipulate genes in different organisms without them needing to be a model organism. With this technology, the lab will be able to knock-out genes in the ticks and understand their functions better, such as insulin signaling or other targets.

“It’s easier than the previous generation’s tools,” Gulia-Nuss said. “It’s not easy, but definitely easier.”

Lyme disease and public health

“Lyme disease is one of the most important vector-borne disease in the United States,” Gulia-Nuss said. “CDC reports around 300,000 new cases of Lyme disease annually, mostly in the 14 states in the Northeast and Midwest.”

Lyme disease is a tick-borne disease as the bacteria that causes it is carried by the tick. Ticks are blood-feeding organisms and they must feed on vertebrate blood at every developmental stage.

“Ticks go from eggs to larvae, to nymphs to adults, and at every developmental stage, they have to take a blood meal; it’s the only thing that they eat, they do not feed on anything else,” Gulia-Nuss said.

When ticks take this blood meal, they are likely to become infected with pathogens including the Lyme disease bacteria from an infected vertebrate, and transmit it during their next feed.

While Lyme disease is treatable through an antibiotics course, it can be fatal and lead to neuro-degenerative disorders if left untreated. Though Lyme disease is a serious problem, it is not the sole focus of the lab.

“Lyme disease is not the only disease that these ticks carry,” Gulia-Nuss said. “They also carry a number of different viruses, and understanding the tick-pathogen interaction on a molecular level will allow the research community to find new targets for tick control or blocking pathogen transmission.”

Gulia-Nuss’ lab already has support from the research community and this proposal was supported by researchers working on ticks as well as tick-pathogen interactions through letters of support. Once Gulia-Nuss’ lab have these tools made, they are hoping that it will not only help the tick research community, but also public health in general.

“This grant really puts us on the path forward, we are able to hire more staff for the lab, including a graduate student and a post-doctorate, and it will provide money for the next two years for things such as supplies, related costs to the ongoing project and also travel,” Gulia-Nuss said.

Gulia-Nuss received her bachelor’s, masters and doctorate degrees in biosciences from Maharshi Dayanand University in Rohtak, India. She was a research scientist at Purdue University before moving to the University of Nevada, Reno as an assistant professor in 2016.

 

 

Wolbachia-Laced Mosquitoes Being Released & Why Lyme/MSIDS Patients Might be Negatively Affected

 Inside Edition Published Feb. 11, 2018

https://www.naturalnews.com/2018-02-11-mosquitoes-infected-with-natural-bacteria-prevent-reproduction-released-in-miami.html

The Miami-Dade Country Mosquito Reduction Test Program, a collaboration between the University of Kentucky and biotech company MosquitoMate, is releasing lab-bred mosquitoes infected with Wolbachia into the wild to supposedly depopulate Aedes aegypti mosquitos that carry dengue fever, yellow fever, and Zika. They are conducting an initial test phase to see if it can become operational.

Wolbachia stops mosquitoes from reproducing.  The eggs die before they hatch.

Here are some potential problems:

  1. What if Wolbachia causes a mutation?
  2. Evidently, consent has not been given.  Humans live here.
  3. Dogs treated for Heart Worm have severe inflammation due to released Wolbachia in the blood stream
  4. Wolbachia enhances other pathogens

https://madisonarealymesupportgroup.com/2017/07/10/wolbachia-the-next-frankenstein/  Wolbachia, a Gram-negative bacterium of the family Rickettsiales first found in 1924 and in 60% of all the insects, including some mosquitoes, crustaceans, and nematodes (worms). It was largely unknown until the 90’s due to its evasion tactics.  It has been used in human diseases such as elephantiasis and River Blindness, both caused by filiarial nematodes.

Wolbachia’s favorite hosts are filarial nematodes and arthropods.

Here’s where it gets tricky.  It is commonly known that nematodes (worms) are often a part of the Lyme/MSIDS patient picture & explains the importance of the following animal study.

Dogs treated for heart worm (D. immitis) have trouble due to the heart worm medication causing Wolbachia to be released into the blood and tissues causing severe Inflammation in pulmonary artery endothelium which may form thrombi and interstitial inflammation. Wolbachia also activates pro inflammatory cytokines. Pets treated with tetracycline a month prior to heart worm treatment will kill some D. immitis as well as suppress worm production. When given after heart worm medication, it may decrease the inflammation from Wolbachia kill off.  http://www.critterology.com/articles/wolbachia-and-their-role-heartworm-disease-and-treatment
The words worms and inflammation should cause every Lyme/MSIDS patient to pause. Many of us are put on expensive anthelmintics like albendazole, ivermectin, Pin X, and praziquantel to get rid of worms and are told to avoid anything causing inflammation due to the fact we have enough of it already. We go on special anti-inflammatory diets and take systemic enzymes and herbs to try and lower inflammation. https://madisonarealymesupportgroup.com/2016/04/22/systemic-enzymes/

Seems to me, many MSIDS/LYME patients when treated with anthelmintics, will have Wolbachia released into their blood and tissues causing wide spread inflammation, similarly to dogs.

And that’s not all.

According to a study by Penn State, mosquitoes infected with Wolbachia are more likely to become infected with West Nile – which will then be transmitted to humans.“This is the first study to demonstrate that Wolbachia can enhance a human pathogen in a mosquito,“ one researcher said. “The results suggest that caution should be used when releasing Wolbachia-infected mosquitoes into nature to control vector-borne diseases of humans.” “Multiple studies suggest that Wolbachia may enhance some Plasmodium parasites in mosquitoes, thus increasing the frequency of malaria transmission to rodents and birds,” he said. https://www.sciencedaily.com/releases/2014/07/140710141628.htm

So besides very probable wide spread inflammation, and that other diseases may become more prevalent due to Wolbachia laced mosquitoes, studies show Wolbachia enhances Malaria in mosquitos.

Lyme/MSIDS patients are often co-infected with Babesia, a malarial-like parasite that requires similar treatment and has been found to make Lyme (borrelia) much worse.

Lastly, with Brazil’s recent explosion of microcephaly, the introduction of yet another man-made intervention (Wolbachia laced mosquitos) should be considered in evaluating potential causes and cofactors. And while the CDC is bound and determined to blame the benign virus, Zika, there are numerous other factors that few are considering – as well as the synergistic effect of all the variables combined. Microcephaly could very well be a perfect storm of events.
https://madisonarealymesupportgroup.com/2016/12/21/how-zika-got-the-blame/, https://madisonarealymesupportgroup.com/2016/03/04/health-policy-recap/, https://madisonarealymesupportgroup.com/2016/03/08/fixation-on-zikapolio/

I hate bugs as much as the next person, but careful long-term studies of Wolbachia are required here.

Hopefully it is evident that many man-made interventions have been introduced into the environment causing important health ramifications: Wolbachia laced mosquitoes and eggs, GMO mosquitoes including CRISPR, and in the case of Zika in Brazil, whole-cell pertussis vaccinations (DTap) for pregnant women up to 20 days prior to expected date of birth, a pyriproxyfen based pesticide applied by the State in Brazil on drinking water, as well as aerial sprays of the insect growth regulators Altosid and VectoBac (Aquabac, Teknar, and LarvX, along with 25 other Bti products registered for use in the U.S.) in New York (Brooklyn, Queens, Staten Island, and The Bronx) to combat Zika. “We feel it’s critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome … Researchers who aren’t using whole genome sequencing to find off-target effects may be missing potentially important mutations. Even a single nucleotide change can have a huge impact.http://articles.mercola.com/sites/articles/archive/2017/06/13/crispr-gene-editing-dangers.aspx?utm_source=dnl&utm_medium=email&utm_content=art3&utm_campaign=20170613Z1_UCM&et_cid=DM147520&et_rid=2042753642

All of this is big, BIG business.

Is the introduction of Wolbachia another puzzle piece in the perfect storm of events causing or exacerbating human health issues?
The jury’s still out, but it’s not looking good – particularly for the chronically ill.

https://articles.mercola.com/sites/articles/archive/2018/02/13/lab-made-mosquitoes-released-in-miami.aspx?  “If preventing Zika was their aim, government officials missed the boat on this one; although Miami-Dade County was previously designated as a Zika cautionary area, that designation was removed June 2, 2017.  No Zika virus disease cases have been reported with illness onset in 2018 in the U.S., while in 2017 there were only four cases of Zika virus reported that were presumably acquired via local mosquitoes (two in Florida and two in Texas).  There is a major push to combat mosquito-borne diseases in the continental U.S. with the use of lab-made and GE mosquitoes, even though in the U.S. mosquito-borne illnesses are not a grave threat, especially compared to other major public health crises like the opioid epidemic.”

And I will add the tick borne illness crisis, which truly is a pandemic.

 

 

 

 

 

 

 

Connecting the Dots of Yolanda’s Lyme Experience

https://www.lymedisease.org/touchedbylyme-yolanda-hadid-book/  by Dorothy Kupcha

TOUCHED BY LYME: Connecting the dots of Yolanda’s Lyme experience

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I first learned about the Lyme disease experiences of Yolanda Hadid (then known as Yolanda Foster) via Twitter.

At that point, Yolanda was a cast member of the “Real Housewives of Beverly Hills” TV show, a former high fashion model, wife of millionaire music mogul David Foster, and mother to three children who would themselves go on to high profile careers in modeling.

I admit, her story hooked me right away and I immediately started following her Twitter posts. Her tweets offered a trail of tantalizing bread crumbs. They alluded to hyperbaric oxygen, stem cells, hyperthermia treatments and various cleanses and detoxification protocols. Yet, details were non-existent. She never gave the reader any solid information about her symptoms, nor her wide and varied treatment protocols.

Eventually, she would write blogs for the Bravo website, in connection with the Housewives show. These occasionally mentioned Lyme disease. There were media interviews that spoke of some of her difficulties, and a brilliant speech at the 2013 Time for Lyme Gala in Connecticut.

But mostly, her story dribbled out as a string of cryptic comments on social media. They typically raised more questions than they answered.

Now, Yolanda has connected the dots for us in her book, “Believe Me: My Battle with the Invisible Disability of Lyme Disease.” (St. Martin’s Press, 2017)

It’s a compelling read. Lyme patients will identify with many of its elements: troubling physical symptoms that can’t be explained; a long, traumatic search for an accurate diagnosis, with plenty of missteps by top medical doctors; the difficulties of treatments, both traditional and alternative.

Not everything is something the rest of us might relate to, however. Before she gets sick, Yolanda and David Foster inhabit a glamorous, jet-setting realm, which includes her involvement with the “Real Housewives” TV show.

However, all that changes as her health fails and she must marshal every ounce of inner strength she has to save her life and her sanity. Yolanda falls further and further away from the dazzling world of the entertainment industry, and eventually her marriage collapses as well.

Her willingness to keep searching for answers is a major theme of “Believe Me.” By this time, two of her children are also being treated for Lyme disease. She fights for their lives as well as her own. And in the midst of it, she loses her dear friend Ellie to the ravages of ALS—a severe emotional blow.

Through it all, Yolanda perseveres. She crisscrosses the globe to try out an astonishing array of alternative and ancillary treatments. She has metal-based crowns removed from her teeth and toxin-leaking implants removed from her breasts. She pursues the mystery of intestinal parasites, eventually expelling some gnarly looking rope worms. (Color photos included!)

I don’t view “Believe me” as a road map for Lyme disease treatment. Rather, it’s an inspiring description of her personal journey. Despite many twists and turns, it ultimately leads her to a good place.

I salute Yolanda for the grace, courage, and fortitude with which she endured an incredibly difficult stage of her life. And I thank her for so generously sharing what she has learned along the way.

TOUCHED BY LYME is written by Dorothy Kupcha Leland, LymeDisease.org’s VP for Education and Outreach. She is co-author of When Your Child Has Lyme Disease: A Parent’s Survival Guide. Contact her at dleland@lymedisease.org

____________

**Comment**

I have not read Hadid’s book yet but am thankful the parasite/worm issue was broached as many Lyme/MSIDS patients improve after taking anthelmintics such as Albenza, Ivermectin, and pin worm medication. Microbiologist Tom Greer shows that Burgdorferi and miyamotoi are associated with amyloid plaques in Alzheimer’s brainsBorrelia found in Lewy Body Dementia, nematodes (worms) found in Alzheimer’s brains, and Borrelia found in five deadly brain tumors (Glioblastoma multiform).  https://madisonarealymesupportgroup.com/2016/08/09/dr-paul-duray-research-fellowship-foundation-some-great-research-being-done-on-lyme-disease/

Pathologist Alan McDonald has found three strains of borrelia living in parasitic nematode worms, worm eggs, or larvae in the brain tissue of 19 autopsies.
MacDonald states that both worms and borrelia can cause devastating brain damage and that “while patients are wrongly declared free of Lyme and other tick-borne infections, in reality, too often they contract serious neurodegenerative diseases which can kill them.”  

Lyme discoverer, Willy Burgdorfer, wrote of finding nematodes in tick guts way back in 1984 and in 2014 University of New Haven researcher, Eva Sapi, found 22% of nymphs and 30% of adult Ixodes ticks carried nematodes.  https://madisonarealymesupportgroup.com/2016/06/03/borrelia-hiding-in-worms-causing-chronic-brain-diseases/  

Parasite treatment:  https://madisonarealymesupportgroup.com/2017/10/03/removing-parasites-to-fix-lyme-chronic-illnesses-dr-jay-davidson/

After reading about symbionts found in ticks and worms, https://madisonarealymesupportgroup.com/2017/05/01/co-infection-of-ticks-the-rule-rather-than-the-exception/, I am concerned the use of Wolbachia (a symbiont) as a biocontrol as it could cause widespread inflammation in Lyme/MSIDS patients:  https://madisonarealymesupportgroup.com/2017/07/10/wolbachia-the-next-frankenstein/  Dogs treated for heart worm (D. immitis) have trouble due to the heart worm medication causing Wolbachia to be released into the blood and tissues causing severe Inflammation in pulmonary artery endothelium which may form thrombi and interstitial inflammation. Wolbachia also activates pro inflammatory cytokines.

 

 

 

Misdiagnosed: How Children With Treatable Medical Issues Are Mistakenly Labeled as Mentally Ill

https://www.huffingtonpost.com/entry/misdiagnosed-how-children-with-treatable-medical-issues_us_59d6b302e4b0705dc79aa68f by A. Elizabeth Washington, Writer, Advocate, Mother

Misdiagnosed: How Children With Treatable Medical Issues Are Mistakenly Labeled as Mentally Ill

10/05/2017 

In the fall of 2015, eleven-year-old Sophia Cahill* began blinking her eyes. Though an eye doctor dismissed the blinking as a symptom of dry eyes, her parents would look back later and realize the blinking was a tic. Sophia was otherwise healthy and unbothered by the blinking so life carried on as usual. The simple tic would unfortunately foreshadow much darker days to come.

As Sophia entered seventh grade the following year, she enjoyed spending time with friends and family, performed well academically, and excelled in several sports. She played softball and skied black-diamond slopes with ease. With a love of horseback riding, she had spent two weeks the prior summer at an overnight riding camp. Independent and responsible, she had flown alone across the country to see her cousins and was a trustworthy babysitter for her siblings. Sophia was happy and healthy, with a precocious sense of humor and an easygoing demeanor. Sophia’s parents, both medical doctors, had no concerns about her behavior or health that could have predicted that her life would soon be dramatically and abruptly turned upside down.

Shortly after the school year started, Sophia became sick with a virus and then pneumonia. The illnesses would have been easily forgotten were it not for the troubling episodes that began the following month. Out of the blue and generally in the evenings, Sophia would become extremely distressed and inconsolable, crying for hours at a time. In a state of extreme anguish, she’d rip up boxes of Kleenex, pound her fists on the bed, and repeat bizarre and senseless phrases. Her pupils would dilate and with sheer terror in her eyes and panic on her face, she would scream “Mommy! Mommy, help me!” but no amount of consoling could ease her suffering. Eventually, her hysterical sobbing was punctuated with the disturbing sight and sound of the usually calm twelve-year-old banging her head against the wall. By the wee hours of the morning, she would collapse from utter exhaustion and fall sleep.

The morning after each episode, Sophia would awake in good spirits showing no signs of the turmoil that had transpired the night before. A few nights would pass before another episode would occur. Gradually the episodes became more frequent and began lasting longer. Within three months, she had racked up a number of mental health diagnoses from several different doctors and had started an SSRI, yet her mental health continued to deteriorate.

Shortly after the New Year, the distressing symptoms that Sophia had exhibited only intermittently in the prior months turned into an around-the-clock nightmare for her and her family. With the addition of peculiar involuntary movements and constant moaning that would later be recognized as a vocal tic, Sophia was admitted into the hospital.

While hospitalized, her mother received a call from the pediatrician. The strep titers that she had asked the pediatrician to order were positive. This indicated that Sophia had likely had a fairly recent strep infection. Coupled with her dramatic neuropsychiatric deterioration, the pediatrician believed her mother’s suggestion that Sophia might have pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, commonly referred to as PANDAS, was likely accurate. She asked that Sophia’s mother discuss the possibility with the doctors at the hospital. Because Sophia also had a virus and pneumonia in the month before her symptoms began, pediatric acute-onset neuropsychiatric syndrome, or PANS, was also a consideration. PANDAS, a subset of PANS, requires documentation of previous strep infection. Diagnosis of PANS does not require identification of a specific trigger.

Sophia’s parents shared the labs and their suspicions with the hospital, but the attending physicians were adamant that Sophia did not have PANS. Relentlessly symptomatic, Sophia was transferred to an inpatient child and adolescent unit at another hospital with a diagnosis of anxiety. Here too, her symptoms continued to worsen and she developed an extreme startle response, jerking violently at the slightest sound. One week passed and high doses of anti-psychotics, beta-blockers, and other medications as well as additional investigation into medical causes produced no relief. Desperate for help, Sophia’s parents brought her back to the first hospital.

An MRI, EEG, and lumbar puncture provided no insight into what might be wrong and a neurologist reported she could find nothing amiss neurologically. After seeing another psychiatrist, Sophia picked up yet another diagnosis. This time her parents were told she had a conversion disorder and that they were to bring her home and behave as though nothing was wrong with her. With that, Sophia was discharged from the hospital.

At home, she continued to moan around the clock, jerked her arms uncontrollably, screamed hysterically, and was frequently catatonic. Frantic for answers, Sophia’s parents took her to yet another psychiatrist. This time she was diagnosed with a panic disorder, and though the psychiatrist admitted he honestly was not sure what was wrong with her, he prescribed two different anti-psychotics in an effort to stabilize her.

The attempt failed and by February, Sophia had refused to eat or drink for a full week. Treated for dehydration and released by the hospital, she was sent to an in-patient psychiatric facility. She was initially placed on an eating disorder unit and then moved to the OCD and anxiety unit. The two psychiatrists who evaluated her quickly encouraged her parents to have Sophia evaluated by a doctor who specialized in PANS and PANDAS. Sophia and her parents traveled out of state to see a specialist. With a virus and pneumonia preceding her initial neuropsychiatric symptoms, as well as positive streptococcus titers, the specialist confidently diagnosed Sophia with PANS and its subset PANDAS. Returning to the psychiatric facility with a proper diagnosis and treatment plan in place, Sophia was discharged.

Still suffering horrifically, Sophia tried to end her own life two days later. She was rushed back to the same hospital that had encouraged her parents to take her home and behave as though nothing was wrong the month before.

Now open to the possibility of PANS, hospital physicians agreed to treat her with intravenous immunoglobulin, or IVIG. Derived from the plasma of over a thousand donors, IVIG is used to treat a number of serious and life threatening medical conditions, including PANS. Sophia also underwent plasmapheresis, a procedure in which the plasma is separated from the blood cells, treated to remove auto-antibodies that may be attacking the body, and then returned to the body. Next she received Rituximab, a medication that halts autoimmune disorders by targeting and destroying B-cells, a type of blood cell responsible for antibody production

Though patients receiving these treatments often wait eight or more weeks for relief, Sophia was well enough to leave the hospital by the end of the month. Just as she was beginning to resume a few normal activities, pharyngitis caused relapse and she was readmitted to the hospital for an additional six weeks of aggressive immunomodulatory therapies, antibiotics, tonsillectomy and adenoidectomy. This time, the treatment would provide complete remission.

Four months after her final release from the hospital, Sophia is functioning just as well today as she had been prior to the onset of PANS. She is content, doing well academically, and on the school volleyball team. Surrounded by friends to celebrate her thirteenth birthday last month, Sophia showed no evidence of the year-long nightmare she had endured.

To understand how the physicians of a highly regarded hospital system could repeatedly misdiagnose Sophia, it is helpful to understand the history of PANS and PANDAS. National Institute of Mental Health researcher, Dr. Susan Swedo, first recognized what would come to be called PANDAS more than 25 years ago. While researching Sydenham’s chorea and obsessive-compulsive disorder (OCD), the mother of a patient with severe OCD and tics mentioned that her son had strep throat less than two weeks before his onset of symptoms. She had also noticed her older son’s tics would worsen a couple days before the start of a sore throat and positive strep test. As Dr. Swedo investigated further, she became aware that other infections also triggered OCD, tics, psychiatric issues, and behavioral problems in certain children.

Focusing early research on strep-triggered cases of obsessive-compulsive and tic disorders, Dr. Swedo published a paper in 1998 that provided clinical description of the first 50 children she had observed with PANDAS. All cases were characterized by an abrupt onset of OCD or tics following a strep infection. Many of the children also suffered from emotional lability, changes in school performance, personality changes, bedtime fears, separation anxiety, irritability, sensory defensiveness, impulsivity, distractibility, deterioration in handwriting and math skills, oppositional defiant behaviors, and nightmares (1).

A small handful of neurologists were swift to criticize the research. Quickly labeled as controversial, Dr. Swedo and other researchers would find themselves defending the concept of PANS for decades to come. Ruthless in their attack of PANS and PANDAS, several critics published a paper in 2012 in the Journal of Pediatrics titled “Moving From PANDAS to CANS (2).” Despite a large body of evidence to the contrary, they again called into question the scientific evidence for its existence. They also criticized the use of antibiotics to treat children with abrupt onset OCD and tics despite evidence that the health of many children with PANS was restored with antibiotic treatment.

After the paper was published, it was revealed that three of the authors, Dr. Roger Kurlan, Dr. Harvey Singer, and Dr. Donald Gilbert, failed to disclose that they had received financial support from the pharmaceutical company Psyadon (3). The company manufactures a medication for tics, providing a possible motive for their persistent criticism of the concept of PANS and use of inexpensive antibiotics to treat it.

Despite the frequent negative publicity, significant progress has been made in the understanding and treatment of PANS. In 2012, Lucile Packard Children’s Hospital at Stanford started a program treating children with PANS. In 2013, they hosted a conference with a number of experts from prestigious medical institutions and published a paper with clear diagnostic guidelines (4). In February 2015, an entire edition of the Journal of Child and Adolescent Psychopharmacology (5) was dedicated to PANS and PANDAS and in 2017, the same journal published three articles detailing full treatment guidelines (6). The articles were co-authored by an incredible team of experts like Dr. James Leckman, Professor of Child Psychiatry at Yale University, who served as the Director of Research for the Yale Child Study Center for more than twenty years; Dr. Mark Pasternack, infectious disease doctor and Associate Professor of Pediatrics at Harvard University; Dr. Jennifer Frankovich, PANS rheumatologist and Director of the PANS Program at Stanford; and more than two dozen other experts from prominent institutions.

Though experts consider the controversy to be resolved, the vast majority of pediatricians, child psychiatrists, and neurologists are unapprised of the latest research and continue to misdiagnose children who have PANS with any number of mental health disorders. The PANDAS Physician Network, an organization that educates medical professionals and sponsors research of the disorder, lists only one or two physicians who treat PANS in many states. Considering that by National Institute of Mental Health estimates, at least 350,000 children in the United States have PANS, the number of doctors who recognize and treat it is woefully inadequate to meet the needs of suffering children.

For now, many children with PANS continue to wait for the medical community to catch up to what experts have known for decades. We can only hope they’ll be as lucky as Sophia and receive proper medical attention before it’s too late.

 

*Name has been changed to protect privacy.

 

References

1. Swedo, Susan E., et al. “Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases.” American Journal of Psychiatry 155.2 (1998): 264-271.

2. Singer, Harvey S., et al. “Moving from PANDAS to CANS.” The Journal of pediatrics 160.5 (2012): 725-731.

3. Singer, Harvey S., et al. “Moving from PANDAS to CANS.” The Journal of pediatrics 160.5 (2012): 725-731. (see correction)

4. Chang, Kiki, et al. “Clinical evaluation of youth with pediatric acute-onset neuropsychiatric syndrome (PANS): Recommendations from the 2013 PANS Consensus Conference.” Journal of Child and Adolescent Psychopharmacology 25.1 (2015): 3-13.

5. Chang, Kiki, Harold S. Koplewicz, and Ron Steingard. “Special issue on pediatric acute-onset neuropsychiatric syndrome.” Journal of child and adolescent psychopharmacology 25.1 (2015): 1-2.