Archive for the ‘Borrelia Miyamotoi (Relapsing Fever Group)’ Category

Where Ticks Are and What They Carry – Science Conversation With Dr. Cameron

http://danielcameronmd.com/lyme-disease-science-conversation-ticks-diseases-they-carry/  Approx. 50 Min

Dr. Daniel Cameron, a leading Lyme disease expert, discusses where are the ticks and what are the diseases they carry.

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**Comment**

The word is finally getting out.  TICKS ARE EVERYWHERE!

Beaches:  https://madisonarealymesupportgroup.com/2018/06/07/ticks-on-beaches/

Rocks and picnic benches:  https://madisonarealymesupportgroup.com/2017/03/13/ticks-found-on-rocks/

Caves:  https://madisonarealymesupportgroup.com/2018/04/23/tick-borne-relapsing-fever-found-in-austin-texas-caves/, and https://madisonarealymesupportgroup.com/2017/10/27/israeli-kids-get-lyme-disease-from-ticks-in-caves/

Birds:  https://madisonarealymesupportgroup.com/2017/08/17/of-birds-and-ticks/

California:  https://madisonarealymesupportgroup.com/2018/05/19/infected-ticks-in-california-its-complicated/

In the South:  https://madisonarealymesupportgroup.com/2018/05/31/no-lyme-in-the-south-guess-again/, and https://madisonarealymesupportgroup.com/2017/10/06/remembering-dr-masters-the-rebel-for-lyme-patients-who-took-on-the-cdc-single-handedly/, and https://madisonarealymesupportgroup.com/2017/03/02/hold-the-press-arkansas-has-lyme/

Southern Hemisphere:  https://madisonarealymesupportgroup.com/2018/02/06/lyme-in-the-southern-hemisphere-sexual-transmission/

Australia:  https://madisonarealymesupportgroup.com/2016/11/03/ld-not-in-australia-here-we-go-again/

And everywhere else…..

Remember, there are 300 strains and counting of Borrelia worldwide and 100 strains and counting in the U.S.  Current CDC two-tiered testing tests for ONE strain!  Do the math….

For more:  https://madisonarealymesupportgroup.com/2018/05/27/study-conforms-permethrin-causes-ticks-to-drop-off-clothing/

https://madisonarealymesupportgroup.com/2018/06/06/mc-bugg-z/

 

 

 

 

Update on TBD’s in Travelers

https://www.ncbi.nlm.nih.gov/m/pubmed/29789953/

Update on Tick-Borne Bacterial Diseases in Travelers.

Review article

Eldin C, et al. Curr Infect Dis Rep. 2018.

Abstract

PURPOSE OF REVIEW: Ticks are the second most important vectors of infectious diseases after mosquitoes worldwide. The growth of international tourism including in rural and remote places increasingly exposes travelers to tick bite. Our aim was to review the main tick-borne infectious diseases reported in travelers in the past 5 years.

RECENT FINDINGS: In recent years, tick-borne bacterial diseases have emerged in travelers including spotted fever group (SFG) rickettsioses, borrelioses, and diseases caused by bacteria of the Anaplasmataceae family. African tick-bite fever, due to Rickettsia africae, is the most frequent agent reported in travelers returned from Sub-Saharan areas. Other SFG agents are increasingly reported in travelers, and clinicians should be aware of them. Lyme disease can be misdiagnosed in Southern countries. Organisms causing tick-borne relapsing fever are neglected pathogens worldwide, and reports in travelers have allowed the description of new species. Infections due to Anaplasmataceae bacteria are more rarely described in travelers, but a new species of Neoehrlichia has recently been detected in a traveler. The treatment of these infections relies on doxycycline, and travelers should be informed before the trip about prevention measures against tick bites.

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**Comment**

This review clearly shows how much work still needs to be done.  To boil down this complex illness to a round of doxycycline shows a simplistic understanding of these pathogens on steroids.  Mainstream researchers still haven’t gotten the memo that Eva Sapi reported about doxy throwing the spirochete into the non-cell wall form or the information that both pathologist Alan McDonald and microbiologist Tom Greer are finding spirochetes hiding in worms in the brains of folks with dementia and Alzheimer’s.

To announce doxy as the “one side fits all” treatment is truly uninformed.

While doxy is a great front-line drug, patients need to be monitored closely for symptoms.  Since testing is so poor, doctors should also be educated on:  https://madisonarealymesupportgroup.com/2017/09/05/empirical-validation-of-the-horowitz-questionnaire-for-suspected-lyme-disease/  Print out and complete the symptom check lists and take them with you to your appointment.

Remember, Lyme is the rock star we all know by name.  There are many wanna-be’s just as powerful often at play:  https://madisonarealymesupportgroup.com/2017/07/01/one-tick-bite-could-put-you-at-risk-for-at-least-6-different-diseases/  The number is actually 18 and counting.

Please encourage doctors to become educated.  It’s our only hope.

https://madisonarealymesupportgroup.com/2018/02/19/calling-all-doctors-please-become-educated-regarding-tick-borne-illness-heres-how/

Here is an example of good Lyme treatment:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

Type other pathogens into the search bar to get other treatment suggestions.  Feel free to copy these off and share with your practitioner.

 

 

 

 

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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First Detection in Italy of Borrelia Miyamotoi in Ixodes Ricinus Ticks

https://www.ncbi.nlm.nih.gov/m/pubmed/29554975/

First detection of Borrelia miyamotoi in Ixodes ricinus ticks from northern Italy.

Ravagnan S, et al. Parasit Vectors. 2018.

Abstract

BACKGROUND: Borrelia miyamotoi is a spirochete transmitted by several ixodid tick species. It causes a relapsing fever in humans and is currently considered as an emerging pathogen. In Europe, B. miyamotoi seems to occur at low prevalence in Ixodes ricinus ticks but has a wide distribution. Here we report the first detection of B. miyamotoi in Ixodes ricinus ticks collected in two independent studies conducted in 2016 in the north-eastern and north-western Alps, Italy.

RESULTS: Three out of 405 nymphs (0.74%) tested positive for Borrelia miyamotoi. In particular, B. miyamotoi was found in 2/365 nymphs in the western and in 1/40 nymphs in the eastern alpine area. These are the first findings of B. miyamotoi in Italy.

CONCLUSIONS: Exposure to B. miyamotoi and risk of human infection may occur through tick bites in northern Italy. Relapsing fever caused by Borrelia miyamotoi has not yet been reported in Italy, but misdiagnoses with tick-borne encephalitis, human granulocytic anaplasmosis or other relapsing fever can occur. Our findings suggest that B. miyamotoi should be considered in the differential diagnosis of febrile patients originating from Lyme borreliosis endemic regions. The distribution of this pathogen and its relevance to public health need further investigation.

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**Comment**

That last sentence is the understatement of the year.  Unfortunately, Science is in the Dark Ages regarding all things Lyme/MSIDS with experts clinging to ancient, dusty, and often unscientific research that desperately needs updating.

https://madisonarealymesupportgroup.com/2018/03/11/italy-5-year-tick-survey/  It appears our Italian friends now are on record for having Rickettsia species, Anaplasma, & Bartonella.

19554184_1928116994100157_3435542982596343683_n

My daughter in Rome, Italy

Please remember that up until 1994 B. miyamotoi wasn’t even on the radar except in Japan and there it was in Ixodes persulcatus ticks.  Human cases weren’t reported until 2011 in Russia and then the U.S., Europe, and Japan.  Think of all the patients who presented with severe illness but went undiagnosed.  This is still happening.  

https://www.ncbi.nlm.nih.gov/m/pubmed/25892254/?i=2&from=/28714333/related

B. miyamotoi species are usually transmitted by soft-bodied ticks or lice; however, it has been found in at least six Ixodes tick species in North America and Eurasia that transmit Lyme as well.  A great reminder that we need to be very careful about being closed-minded regarding what ticks carry what.  

Also important to note is the lack of belief of mainstream medicine on the severity, complexity, and length of illness these pathogens can cause.  While it’s true some who are treated quickly get better, others do not and suffer for years with debilitating illness:  https://madisonarealymesupportgroup.com/2018/02/02/hopkins-study-shows-severe-symptoms-in-some-after-lyme-treatment/  (Please read my comment after the study)

Mainstream medicine STILL does not take into account ALL of the pathogens involved.  They test and treat for ONE pathogen, whereas patients are often coinfected with numerous pathogens – including bacteria, viruses, funguses, parasites, and even nematodes (worms).  Until patients are treated for ALL pathogens and a faulty immune system they will not improve.  Again, all the doxy in the world isn’t going to cure this.  https://madisonarealymesupportgroup.com/2017/07/01/one-tick-bite-could-put-you-at-risk-for-at-least-6-different-diseases/  (The actual number is 16 & counting)

 

 

 

 

 

 

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
Tsai GE, Falk WE, Gunther J, Coyle JT: Improved cognition in Alzheimer’s disease with short-term D-cycloserine treatment. Am J Psychiatry. 1999, 156: 467-469.PubMedGoogle Scholar
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:

Wed Nite @ The Lab – Talk on Mosquitoes, Ticks, & Disease


Approx. 1:24:00

Wednesday Nite @ The Lab
Published on Jan 16, 2018

“Susan Paskewitz’s talk will focus on the activities of the newly created Midwest Center of Excellence for Vector-Borne Disease. The center was established in 2017 as a response to the increasing rate of human illness caused by tick and mosquito-transmitted diseases in the region, including Lyme disease and West Nile encephalitis. In addition to these familiar problems, new ticks, mosquitoes, and pathogens have been discovered. Solving these issues will require a new generation of trained vector biologists, cooperation and collaboration among public-health professionals and scientists, and creative and innovative research to reduce human and insect contact.”

About the Speaker

Paskewitz is the director of the Midwest Center of Excellence for Vector-Borne Disease and the chair of the Department of Entomology at UW–Madison. Her research focuses on the ecology, epidemiology, and management of ticks and mosquitoes. She teaches classes in global health, medical and veterinary entomology, and the One Health concept, during which she enjoys working with undergraduate and graduate students who seek to gain experience in public health, infectious disease, and vector-biology research. Paskewitz earned her bachelor’s and master’s degrees at Southern Illinois University–Carbondale and her doctorate at the University of Georgia–Athens.

___________________

Highlights:

4:45 Believe it or not, Wisconsin used to have cases of Malaria.

Zika, discovered in 1947, wasn’t even in our hemisphere. Very few people infected until 2007 when there were 13-14 cases. 2015 it showed up in Brazil. First time a mosquito spread disease that is also sexually transmitted. A medical entomologist felt he gave it to his wife and then wrote a paper on it.

(I guess we need a medical entomologist to infect his/her wife with Lyme/MSIDS so that a paper can be written to prove sexual transmission…..) Please see:  https://madisonarealymesupportgroup.com/2018/02/26/transplacental-transmission-fetal-damage-with-lyme-disease/ and https://madisonarealymesupportgroup.com/2017/02/24/pcos-lyme-my-story/

UW did a lot of work on Zika. Cases in the U.S. occurred when people traveled abroad, became infected, were bit by mosquitoes here, and then spread from there. Only 63 infected people in 2016, 9 more in 2017.

Do we have the mosquitoes that can pick up the virus and transmit it? The Yellow Fever mosquito is the one transmitting Zika. The mosquito is here in U.S. but NOT in WI.  The Asian Tiger mosquito is a secondary vector that transmits the same viruses but not as well. Has a wider distribution and is a daytime feeder.

She looked in all the records – couldn’t find the Asian Tiger in Wisconsin.  It is found in Illinois and Indiana.  However, since that time they have laid many traps and found the Asian Tiger Mosquito here but she doesn’t feel they are abundant or wide spread.  She also feels they won’t survive our winters but experiments are in progress.  Females bite, lay eggs in wet aquatic spots, as larvae need water to grow.

(The same sort of diligence needs to happen in the world of Lyme.  For instance, borrelia has been found in other insects, but entomologists downplay it and say numbers are small.  This is a great example of how Lyme is treated differently then other diseases that are big money-makers for researchers.)

25:32 The Lone star tick has popped up in a number of places in WI – she doesn’t feel they will survive our winters.

Spent a lot of time talking about mosquito issues happening down South.

She admits the Center was created due to Zika.  

(Don’t be shocked when all the research dollars go to Zika & not tick borne illness despite the much higher prevalence of TBI’s in WI)

Wisconsin has cases of West Nile, La Crosse Virus, and Jamestown Canyon Virus – which has increased human cases – they don’t know why.

They are working on a bacterial based topical repellent.  Also working on using fish and copepods to eat mosquitos at the larval stage.

38:00 TICKS

Ticks transmit Lyme Disease – a lot and it’s not just in the North. Could pick it up anywhere in Wisconsin.

Please see:  https://madisonarealymesupportgroup.com/2017/10/06/remembering-dr-masters-the-rebel-for-lyme-patients-who-took-on-the-cdc-single-handedly/

Map showing Deer tick population between 1907-1996 and 1907-2015 –

Our entire state is infested.  

Sky rocket of LD in WI CONFIRMED.  She admits the CDC says the cases are hugely underestimated – more like 30,000 cases per year in WI.

WI is a hotspot for newly emerging TBI – Anaplasma, Ehrlichia muris, borrelia miyamotoi (relapsing fever), Babesia divergens (in Michigan but Paskowitz feels it’s probably here too).

Anaplasma seeing 400-600 cases a year in WI.  Again, much underreporting.

44:00 talks about tick distribution maps.

Please see:  http://steveclarknd.com/wp-content/uploads/2013/11/The-Confounding-Debate-Over-Lyme-Disease-in-the-South-DiscoverMagazine.com_.pdf (go to page 6 and read about Speilman’s maps which are faulty but have ruled like the Iron Curtain, and have been used to keep folks from being diagnosed and treated)

They are working on a way for public to take pictures of ticks, send it to the lab and get answers.

Trying to reduce the risk….they think it’s the nymphs that do most of the transmission because they are tiny and we don’t feel them.

Larvae and nymphs love little rodents
Adults love adults, dogs, and deer

50:00 what we can do to stop LD

52:30 One experiment removed buckthorn – looked like a significant impact after first year but nothing after that.

53:20 tick tubes for micefound a decrease in host-seeking nymphs with this seen it three years running.

Trying to come up with a do it yourself toolkit to implement methods for tick control.

55:55 Working on the tick app – to pool info to show where we are picking up the ticks so education can be more targeted.

ends @ 58:30 then questions

Funding by:  CDC, NIH, USDA, WI Dept HEalth services, WI Dep Natural resources

 

 

 

 

 

Borrelia Miyamotoi Found in Germany

https://www.ncbi.nlm.nih.gov/m/pubmed/29383532/

First report of Borrelia miyamotoi in an Ixodes ricinus tick in Augsburg, Germany.

Page S, et al. Exp Appl Acarol. 2018.

Abstract

Borrelia miyamotoi, a spirochete found in the hard tick Ixodes ricinus, is thought to cause relapsing fever. The disease caused by this bacterium can manifest with high fever, fatigue and other symptoms. It may also lead to central nervous system involvement with symptoms similar to meningoencephalitis. DNA from ticks from the greater Augsburg region in Germany was subjected to qPCR for Borrelia spp., followed by nested PCR and subsequent sequencing for species identification of the qPCR positive samples. From 112 ticks, 20 were found to be positive for Borrelia. The DNA sequenced showed 50% Borrelia afzelli, 15% Borrelia garinii, 5% Borrelia valaisiana and one sequence was identified as Borrelia miyamotoi. The positive identification of Borrelia miyamotoi is unlikely to be due to contamination. In conclusion, Borrelia miyamotoi has been found in a tick in the Augsburg region for the first time. This follows on from previous reports of a low incidence of this bacterium in southern Germany around Lake Constance and in the Munich region. This infectious agent should be taken into account when patients present with recurring fever or neurological symptoms which cannot be otherwise explained. Tick-borne relapsing fever should now be considered as a cause of such symptoms and medical professionals should contemplate differential Borrelia testing when presented with corresponding symptoms.