Archive for the ‘Lyme’ Category

What to Eat When You’re Allergic to Everything?

LYME SCI: What to eat when you’re allergic to everything?

by Lonnie Marcum

What are you going to do, when everything your child eats makes her sick? As I’ve explained in my earlier posts about mast cell activation syndrome (MCAS), virtually anything my daughter put in her mouth triggered a serious allergic reaction.

However, with the help of an incredible medical team and my daughter’s determination to succeed, we found a path to healing. I’m sharing what we did in hopes that it can help others in the same boat.

This is part four of a series on mast cell activation syndrome (MCAS) triggered by Lyme and co-infections. Part one, “When the immune system goes haywire,” serves as an introduction to MCAS; Part two, “The agony of mast cell activation syndrome (MCAS),” reviews the five-step process I used to help my child begin healing from MCAS; Part three, “More about healing from mast cell activation syndrome,” outlines the essentials to finding and eliminating food triggers.

I have been writing for since 2016. This series on MCAS has generated more comments and questions than anything else I’ve written. By far, the most frequent question I’m getting is how to survive a food intolerance crisis.

Today I will share how we got my daughter past her extreme food sensitivities. Future posts will include identifying mold, environmental and cosmetic triggers, how stress affects mast cells and the immune system, and getting your life back.

Food Crisis 101

At the beginning of this MCAS journey, our routine was very stringent. Once we found the right combination of antihistamines, and she was able to go three months without an allergic reaction, we could relax a little. Believe me, I do know what it’s like to be in food crisis, so I’ve laid out a sample of some of our favorite low-histamine foods below to help others learn the process.

In my daughter’s case, the foods we chose were specific for her genetics and their high nutritional value. Her diet is also gluten-free, dairy-free, low in sugar, low-histamine, low-oxalate, and low in sulfites. Depending on your specific needs, you may not need to eliminate all of the above ingredients, or you may need to eliminate these plus others —like foods high in salicylate, a chemical found naturally in certain foods.

The key for us was to make everything from fresh, wholesome, organic ingredients. During her crisis we went with frequent small meals. Because the act of chewing and digesting requires histamine, smaller doses were less triggering. We also eliminated all leftovers, because “aged” foods are higher in bacteria and will trigger more histamine. For a complete list of low-histamine foods click here:

As things improved, I cooked two meals at a time. She’d eat one immediately, I’d refrigerate the other in a glass container (no plastics), and she’d eat the next meal within 3-5 hours. (This allowed me to get other things done.)

We also made sure each meal contained one protein, one carbohydrate and at least one fruit or vegetable. The following are a few suggestions of low-histamine foods that we rotated every three to four days during my daughter’s food crisis. Keep in mind if you are adding new foods the name of the game is low-and-slow, as I laid out in my previous post.

Low Histamine Guidelines (adapted from SIGHI)


  • Fermented products (e.g. alcoholic beverages, vinegar, yeast, bacteria)
  • Produce with uncertain freshness (e.g. packaged chopped lettuce, bean sprouts)
  • Canned, finished or semi-finished products (e.g. canned tuna, meal kits)
  • Reheated food (especially fish, meat and mushroom dishes)


  • Meals from restaurants, snack bars, fast food (due to potential cross contamination of ingredients, uncertain freshness, and uncertain storage time)


  • Wholesome, fresh, unprocessed or lightly processed foods.
  • The more perishable and protein-rich the food, the more important it’s freshness (e.g. fish that is caught, cleaned and flash frozen at sea, then refrigerated uninterruptedly until cooked is best)
  • Leftovers must be refrigerated immediately and eaten within hours or frozen.
This is what worked for us


  • Gluten-free oatmeal, quinoa or white rice with a dash of coconut milk or coconut oil
  • Apple, blueberry, nectarine or peach (baked is easier for her to tolerate)


  • Sautéed meat in extra virgin olive oil (EVOO*) with seasonings**
  • Gluten-free brown rice noodles or quinoa noodles
  • Boiled carrots, cauliflower, broccoli, or peas (I throw them in with the noodles)


  • Baked pumpkin or sunflower seeds (soak 6-8 hours, rinse, bake in EVOO at 300 degrees for15-25 min., till done)


  • Baked meat, coated in EVOO* and seasonings**
  • Baked butternut, acorn or summer squash, sweet potato (the white one)
  • Sautéed arugula, asparagus, butter lettuce, or watercress (boiled artichoke is another good option)

*I use 100% extra virgin olive oil to sauté or bake everything. If you are salicylate-intolerant, you may have trouble with EVOO. Coconut oil and nigella sativa oil (black seed oil) are also recommended.

**Seasonings: Sea salt, pink pepper, ginger, chives, garlic (small amounts), basil, parsley, thyme, rosemary, and sage (dehydrated herbs are more tolerable when in a crisis.)

Note: I am not a doctor. Food allergies are unique to each individual, so it’s important that you work closely with your doctor or a registered dietitian to find and eliminate your food triggers, then design a balanced plan that works for you.

LymeSci is written by Lonnie Marcum, a Licensed Physical Therapist and mother of a daughter with Lyme. Follow her on Twitter: @LonnieRhea  Email her at: .


SIGHI-Leaflet Histamine Elimination Diet Simplified histamine elimination diet for histamine intolerance (DAO degradation disorder)


For the previous articles by Marcum on MCAS:




_______________   Our LLMD uses LDA/LDI for those with immunoconfusion with success.  More about the treatment within this link.  The many benefits of MSM – including allergy symptoms:  

*Reduces cytokines & inflammation (in vitro studies show MSM reduces IL-6 (a marker implicated in chronic inflammation as well as suppressing NO and prostanoids) *antioxidant *free radical scavenger *kills gastrointestinal, liver, and colon cancer cells *restored normal cellular metabolism in mouse breast cancer and melanoma cells *helps wounds heal *increases blood flow *reduces muscle spasms *antiparasitic properties (especially for giardia) *normalizes the immune system *cholinesterase inhibitor *alleviates allergy symptoms *increases energy *improves condition of hair, nails, and skin

Comparative Diets to Address Chronic Inflammation

Comparative Diets to Address Chronic Inflammation


The following is the first half of a two-part article on nutrition that addresses chronic inflammation.

One of the hallmarks of many chronic diseases and disorders is unresolved inflammation in the body. Chronic inflammation can develop when the immune system’s normal inflammatory response to an implied threat continues unabated rather than turning off once the threat is gone.1

Chronic inflammation is a common link among autoimmune disorders like rheumatoid arthritis, lupus and multiple sclerosis; in cardiovascular disorders that lead to heart attacks and strokes; in neurological disorders such as Alzheimer’s, Parkinson’s and epilepsy; and in mental disorders such as depression and schizophrenia.1 Vaccination has been reported to trigger the development of autoimmune disorders associated with chronic inflammation. 2

Infections and Vaccination: Two Different Kinds of Inflammatory Responses and Immunity

Infections and vaccines stimulate different kinds of inflammatory responses in the body to produce antibodies that confer two different kinds of immunity. Naturally acquired active immunity is attained after a person experiences a viral or bacterial infection and the body mounts an inflammatory response to stimulate the production of antibodies and confers long lasting natural immunity. Artificially acquired immunity, which is not identical to naturally acquired immunity, is attained when a person receives a vaccine and the body mounts an inflammatory response to produce antibodies and confers temporary immunity. Booster doses of vaccines to re-stimulate inflammatory responses are often given to lengthen artificial vaccine acquired immunity. 3

Depending upon various genetic, biological and environmental risk factors, some people do not resolve inflammation either after an infection or vaccination and can develop chronic inflammation in the body that leads to chronic health problems.45 In addition to lab altered viruses and bacteria, there are many recognized toxins in childhood vaccines that either singly or in combination cause inflammation in the brain and other parts of the body, including mercury, aluminum, formaldehyde, MSG, antibiotics, polyethylene glycol (antifreeze), squalene, virus like particles and adventitious agents.67

Acute inflammation is easy to recognize: heat, swelling, pain and redness at the site of injury or infection. Chronic inflammation is not quite so obvious, but there are common symptoms that indicate its presence. Some of the most frequently reported include headaches and brain fog, bloating and other digestive problems, joint pain, rashes, fatigue, weight gain, gum disease and mood issues8—many signs familiar to parents of autistic and/or vaccine-injured children.9

Diets Address Chronic Inflammation in Vaccine-Injured Children

The childhood vaccine schedule used in the U.S. has been questioned as a potential factor in the development of inflammatory chronic brain and immune system disorders in children.10

It is an unfortunate fact that those who question the safety of vaccines often “come to the table” following a firsthand experience with a vaccine reaction… in other words, too late to avoid the potentially devastating impact such a reaction can have on their own life or the life of their child. Since conventional medicine rarely acknowledges the connection between vaccination and chronic brain and immune disorders in children, it can be difficult to know where to turn after a vaccine reaction has occurred and there is often lag time before parents find a supportive network. In the search for healing, one of the first avenues explored by parents and doctors specializing in biomedical and holistic health interventions involves nutrition therapy.

Diet is among the most basic of approaches to addressing chronic inflammation. The connection between diet and the risk for developing inflammatory disorders has been recognized for at least 50 years, though studies have been inconclusive about the role played by specific foods and nutrients.11 Nevertheless, harnessing the power of food often can help counteract a chronic inflammatory process and improve some of the related symptoms.

Dietary Fundamentals for Reducing Inflammation

With all the “named” diets available, it can be daunting to decide which direction to turn. Most anti-inflammatory diets share certain basic tenets: avoid sugar and processed foods; stay away from refined flour, wheat, white foods like pasta, rice and bread; and eliminate unhealthy fats. Foods that are often recommended to reduce inflammation in the body are fresh fruits, dark green leafy vegetables, high-quality proteins like cold-water fish, and healthy fats. Some nutritionists suggest that the so-called nightshade foods, which include tomatoes, eggplant, peppers, goji berries and white potatoes, may trigger inflammation in some people,9 and commercial milk products may also cause inflammation in people who are sensitive to lactose or milk proteins.11

Food additives, including dyes, preservatives and artificial flavorings and sweeteners, and high-fructose corn syrup have been pinpointed as problematic for many children with autism spectrum disorders (ASD)12 and some nutritionists suggest avoiding them when trying to reduce systematic inflammation through dietary changes.

The Difference Is in the Details

Some of the most well known diets that surface in an online search for foods that fight inflammation include: the Gut and Psychology Syndrome (GAPS), Paleo, Mediterranean, Atkins, DASH, TLC, Mayo Clinic, Weight Watchers, Raw Food, Keto, The Zone, Whole30, Autoimmune Protocol, Dr. Hyman’s Detox and Dukan…to name just a few.  The annual U.S. News & World Report review of dietary rankings13 and other reviews14of current diet trends can provide an overview for understanding different dietary approaches.

What Do the Experts Say?

The choice of an “anti-inflammatory” diet that limits foods, which have been identified as “pro-inflammatory,” depends on consideration of individual factors, such as specific food sensitivities, personal taste preferences, or the simple desire to try a dietary regimen that sounds interesting.

According to Harvard University’s HealthWatch, “Choose the right foods, and you may be able to reduce your risk of illness. Consistently pick the wrong ones, and you could accelerate the inflammatory disease process.”15 Included in the HealthWatch list of pro-inflammatory foods that should be avoided to reduce inflammation include:

  • Refined carbohydrates, such as white bread and pastries
  • French fries and other fried foods
  • Soda and other sugar-sweetened beverages
  • Red meat (burgers, steaks) and processed meat (hot dogs, sausage)
  • Margarine, shortening, and lard

Anti-inflammatory foods include:

  • Tomatoes
  • Olive oil
  • Green leafy vegetables, such as spinach, kale, and collards
  • Nuts like almonds and walnuts
  • Fatty fish like salmon, mackerel, tuna, and sardines
  • Fruits such as strawberries, blueberries, cherries, and oranges


For More:  In this talk Cyndi O’Meara discusses challenges with wheat.  Diagnosed with MS, Dr. Terry Wahls received the best standard medicine had to offer. After declining to the point of being in a wheel chair, she took matters into her own hands and learned how to properly fuel her body. Using the lessons she learned at the subcellular level, she used diet to cure her MS and get out of her wheelchair.

#LymeWarrior Q&A


by Jennifer Crystal


Q. You once mentioned that a scan helped doctors to learn that you weren’t getting enough oxygen to the left side of your brain. What type of scan was it? And how did doctors know the poor oxygenation was caused by Babesia and not by another tick- borne illness?

A. I have had both MRIs and SPECT scans. It was the SPECT scan that allowed my doctor to specifically see that the left side of my brain was not getting enough oxygen. That SPECT scan was done 11 years ago; you may want to talk to your doctor to see if that is still the most accurate scan you can get.

As I described in my Air Hunger post, Babesia is a parasite that feeds on the oxygen in the red blood cells, depriving the patient of much-needed oxygen. In my case, my doctor knew the infection had flared up again because of the scan. I was also having symptoms of babesia including air hunger, post-exertional fatigue, and hypoglycemia. It’s important that you find a Lyme Literate Medical Doctor (LLMD) who can accurately diagnose and treat you, and who will know your case if and when you relapse.

Q. How long does a Herxheimer reaction last, and is there anything that will help speed up the process or lessen its effects?

A. A Jarish-Herxheimer reaction commonly referred to as a “Herx”, is when bacteria dies off faster than the body can eliminate them, making the patient feel worse before they feel better. This can seem counter-intuitive because when you take medication for an infection, you expect to feel better. But when you’re killing off a lot of spirochetes—especially if you’ve been sick for a long time—a Herxheimer reaction is natural and can be viewed as a good sign that the medication is working.

That said, a Herx can feel awful. Your fatigue is worse, your body feels laden with toxins, and you can barely move from bed except to run to the bathroom. The actual elimination of dead bacteria can be surprisingly intense; the first time I had a Herxheimer reaction, I couldn’t believe how often I was in the bathroom, or what was coming out of me. I can only describe it as “toxic bodily waste.”

For me, Herxheimer reactions tended to last up to a week or two, and then pass. Sometimes they were just a couple days long. It all depends on the patient, though. I know patients who have Herxed for a month or more. No matter how intense your Herxheimer reactions are, though, there are a few things you can do to lessen your suffering. These techniques worked for me:

  • Pulse your medications: Some doctors will have their patients take their antibiotics for a certain number of days or weeks, or then have them stop for a while to allow the body time to eliminate the dead bacteria. Other doctors switch up medications at certain intervals. Personally, I took single day breaks from medication when the Herxheimer reactions were especially intense.
  • Figure out which of your medications is causing the Herxheimer reaction. Herxheimer reactions can be caused by herbal supplements, not just by antibiotics or antimalarial medication. I find it’s best to only change one thing at a time in my own protocol; if I increase a homeopathic drop, I wait awhile to see how that goes before altering the dosage on a medication.
  • Eat foods that are known to help you detox: For me, lemon and onion work well; other patients use apple cider vinegar, or even intravenous Vitamin C, though this last option did not work well for me. Remember, everyone is different and you and your doctor need to figure out what’s best for you.
  • Drink lots of water to help flush your system.
  • Sweat: Those pouring night sweats are annoying, especially when you’re changing pajamas and sheets several times a night, but it means the infection is leaving your body. Some people find that light exercise helps. For me, though, exercise only made me feel worse. Others use infrared saunas to increase sweating. Personally, I can not handle the intense heat.
  • Electrolytes: Because you’re sweating so much, your electrolytes may become depleted. I find it helps to drink an electrolyte-infused beverage (try ones that are just water-based, without added sugar) to keep my sodium and potassium levels balanced. Sweating out spirochetes or parasites isn’t all that different from doing an intense cardiovascular workout, so you should consider how the electrolyte water is helping you to replenish your body.
  • Lymphatic drainage: When I’m herxing, bacteria tends to back up in my head, and my integrative manual therapist does lymphatic drainage and cranial sacral therapy to help open up flow from my brain. He also does neurofascial processing on organs that help the body detox, such as the liver. Note: avoid deep tissue massage at these times since it can hold toxins deeper in your body, making you feel worse.

These are only the detox methods that have worked best for me. There are many others recommended by both patients and doctors. At the 2017 International Lyme and Associated Diseases Society conference in Boston, I heard about curcumin, also known as turmeric, a member of the ginger family that acts as an anti-inflammatory and which has many uses to help mitigate Herxheimer reactions. Talk with your LLMD, and with other patients, about what works best for you.

Q. I know you’ve explained that you can’t give medical advice, but can you please tell me what your protocol was?

A. When you hear a story of someone in remission, it’s natural to want to know what they did to get there. But as I’ve explained in previous posts, telling you my specific protocol (which is ever-changing) is not the point, because every single case of tick-borne illness is different.  Even if your symptoms are similar to mine, our individual cases are guaranteed to be different in terms of how long we were sick, how long we went undiagnosed, whether our infections spread to the central nervous system, where else in the body the infections have spread, whether we have co-infections (and which particular ones), and, most importantly, how we responded to any given treatment. An antibiotic that worked well for me might not work at all for you. My protocol is tailored to my specific case, and yours needs to be, too. You and your LLMD may want to check out Dr. Richard Horowitz’s books Why Can’t I Get Better?and How Can I Get Better? Both books outline specific treatments for specific combinations of tick-borne illnesses.

In closing, let me say that in the past I’ve written about the big picture of what has helped me the most: a combination of medication and homeopathic supplements; nutritional supplements; a gluten-free, sugar-free diet; cognitive behavioral therapy; integrative manual therapy; talk therapy; and neurofeedback. I recommend a holistic or integrative approach that encompasses both Western and Eastern modalities as well as adjunct therapies. I recommend lots of rest and self-care. I recommend seeking out a helpful support system of concerned individuals. Unfortunately, I cannot recommend specific medications, and I hope you will understand that I withhold that information in the hope that you will find the right protocol fly working with your LLMD.

jennifer crystalOpinions expressed by contributors are their own.

Jennifer Crystal is a writer and educator in Boston. She is working on a memoir about her journey with chronic tick-borne illness. Contact her at


For more:

Persistent Borrelia Infection in Patients With Ongoing Symptoms of Lyme Disease

Persistent Borrelia Infection in Patients with Ongoing Symptoms of Lyme Disease

Marianne J. Middelveen 1, Eva Sapi 2OrcID, Jennie Burke 3, Katherine R. Filush 2, Agustin Franco 4, Melissa C. Fesler 5 and Raphael B. Stricker 5,* OrcID

Published: 14 April 2018
(This article belongs to the Special Issue Lyme Disease: The Role of Big Data, Companion Diagnostics and Precision Medicine)

Introduction: Lyme disease is a tickborne illness that generates controversy among medical providers and researchers. One of the key topics of debate is the existence of persistent infection with the Lyme spirochete, Borrelia burgdorferi, in patients who have been treated with recommended doses of antibiotics yet remain symptomatic. Persistent spirochetal infection despite antibiotic therapy has recently been demonstrated in non-human primates. We present evidence of persistent Borrelia infection despite antibiotic therapy in patients with ongoing Lyme disease symptoms. Methods: In this pilot study, culture of body fluids and tissues was performed in a randomly selected group of 12 patients with persistent Lyme disease symptoms who had been treated or who were being treated with antibiotics. Cultures were also performed on a group of ten control subjects without Lyme disease. The cultures were subjected to corroborative microscopic, histopathological and molecular testing for Borrelia organisms in four independent laboratories in a blinded manner. Results: Motile spirochetes identified histopathologically as Borrelia were detected in culture specimens, and these spirochetes were genetically identified as Borrelia burgdorferi by three distinct polymerase chain reaction (PCR)-based approaches. Spirochetes identified as Borrelia burgdorferi were cultured from the blood of seven subjects, from the genital secretions of ten subjects, and from a skin lesion of one subject. Cultures from control subjects without Lyme disease were negative for Borrelia using these methods. Conclusions: Using multiple corroborative detection methods, we showed that patients with persistent Lyme disease symptoms may have ongoing spirochetal infection despite antibiotic treatment, similar to findings in non-human primates. The optimal treatment for persistent Borrelia infection remains to be determined.


Figure 1  (A) Top left:  Darkfield microscopy of blood culture showing live spirochete and spherules.  Magnification 400x.  (B) Botom left:  Fieterle silver stain culture fluid from Case 10 showing live spirochetes  Magnification 1000x.  (D) Bottom right:  Typical dermal filaments from patient with Morgellons disease.  Magnification 100x


For more:

Dr. Frid & Mary Beth Pfeiffer on Fox5

 Approx 7 Minutes.  “Good Day New York” on Fox5 – 4/18

Mary Beth Pfeiffer author of Lyme: The First Epidemic of Climate Change and Dr. Frid discuss Lyme disease, symptoms in children, various co-infections we should be all aware and tested for, and best practices for protecting our kids against ticks.



I’m always thankful for publicity about Lyme/MSIDS, but I have to interject about the premise of Pfeiffer’s new book, which I believe to be false.  According to independent Canadian tick expert John Scott, the issue of global warming or climate change has absolutely NOTHING to do with our current dilemma.

John explains, “This climate change ‘theory’ is all part of a well-planned scheme. Even the ticks are smarter than the people who’ve concocted this thing,” he says.
“Climate change has nothing to do with tick movement. Blacklegged ticks are ecoadaptive, and tolerate wide temperature fluctuations. On hot summer days, these ticks descend into the cool, moist leaf litter and rehydrate. In winter, they descend into the leaf litter, and are comfortable under an insulating blanket of snow. Ticks have antifreeze-like compounds in their bodies, and can tolerate a wide range of temperatures. For instance, at Kenora, Ontario, the air temperature peaks at 36°C and dips to –44°C, and blacklegged ticks survive successfully.
“Ticks are marvellous eco-adaptors. They will be the last species on the planet. Do you see how silly this theory of climate change is as a way to rationalize what’s happening. It’s all a red herring to divert your attention,” he explains.  “The authorities have been using tick expansion and climate change to get research dollars. Climate change is a popular topic right now, and that is a great source of funding for related research. However, any research on ticks and climate change is inconclusive––in essence, there is no validity. The long-range, futuristic projections and statistical models are bogus science because blacklegged ticks have already been found in northern Canada. In fact, we documented blacklegged ticks on migratory songbirds in northern Alberta dating back to 1998. Any allocation of government funding for ticks and climate change research is a complete waste of taxpayers’ money. It will not help Lyme disease patients one iota.”

Scott’s quote above is important for two reasons, 1) he’s independent and doesn’t rely on money making schemes for research 2) this climate change paradigm does absolutely nada to help patients.  

There are so many other topics that need to be addressed!

  1. Is Lyme/MSIDS a STD?
  2. Is it spread congenitally?
  3. Is it spread via breast milk?
  4. Are there other modes of transmission (saliva, urine, etc)?
  5. Acknowledgment of coinfection interaction & then appropriate treatment.
  6. Is Lyme/MSIDS persistent/chronic?
  7. If it’s chronic, appropriate treatment needs to be given.
  8. Why won’t insurance cover this?
  9. Why has Lyme/MSIDS been stymied for over 40 years?
  10. Why do some respond to treatment and others don’t?
  11. What can we do to curb/eliminate ticks that’s safe for our environment?
  12. And on, and on to infinity…….



VL15 Lyme Vaccine – Another Fraud?  by Dr. Jose Lapenta

Hello friends of the DERMAGIC EXPRESS network brings you another hot topic today with respect to LYME DISEASE or CHRONIC ERYTHEMA MIGRANS ….NEW VACCINE VL15 FOR LYME DISEASE … ANOTHER FRAUD? 
The first thing I will remind you, once again, is that in the year 1998 the FDA approved the LYMErix VACCINE to be used against this disease, based on”TARGET” or “DIANA” the proteins of Surface of the BORRELIA BURGDORFERI denominated OspA. The laboratory responsible for marketing the vaccine was GlaxoSmithKline (GSK).
1,400,000 doses were released, and the adverse effects reported by VAERS (ADVERSE EFFECTS REPORTING SYSTEM), which I published in the article STORYS OF VICTIMS OF THE VACCINE FOR THE LYME DISEASE here you can read them.
The vaccine resulted in the death of at least 229 people, of whom 43 were SUICIDATED 7 months after receiving the 2nd dose. 

The main side effect was ARTHRITIS, especially the patients with HISTOCOMPATIBILITY ANTIGEN CLASS II, HLA DR4, the laboratory omitted this data in the vaccination, ALSO THE VACCINE DETERIORATED the health of the carriers of the DISEASE. The laboratory also omitted this fact. 

At the end, the LYMErix vaccine was discontinued in 2002 for three reasons: 
And again you’ll be wondering why I’m telling you this HISTORY THAT HAS 15 YEARS OF EVOLUTION. I’ll give you the answer clear and precise !!!!
All this I am explaining to you because throughout these 15 years, THE LYME DISEASE has spread widely in the United States and Europe. In 2008, 440,000 new cases were reported in the United States and 85,000 in Europe. Currently, in 2017, 300,000 new cases are reported annually in the United States according to the CDC (Center for Disease Control and Prevention).
On the other hand, as I already explained, LYME DISEASE, due to the biological characteristics of BORRELIA (SPIROCHETA), which becomes “undetectable” to diagnostic tests, has become a health problem in these countries. An antibiotic treatment costs between $20 and $1000, and INSURANCE COMPANIES DO NOT WANT TO KNOW ABOUT CHRONIC DISEASES, BECAUSE THE COST IS VERY HIGH. Crude reality.
Here comes the GHOST of the LIMErix vaccine and a new FRENCH BIOTECHNOLOGY company, named VALNEVA, who proudly presented on April 11, 2017 at the World Congress on Vaccines, the project of a “NEW” vaccine for LYME DISEASE, called With CODE VL15-101. 

The FDA approved on 9 December 2016, the preliminary tests, leaving pending FINAL APPROVAL based on SUCCESS or failure thereof. The study began in 2016 in Europe, Belgium and will be performed this year 2017 in the United States, in 180 healthy people over 40 years (See attached).
HERE I PUT YOU WHAT VALNEVA SAYS ABOUT THE VL15 PROJECT (See attached)===============================================================
“… Valneva’s vaccine candidate is based on OspA, one of the most dominant surface proteins expressed by the bacteria when present in a tick. The target indication for Valneva’s vaccine candidate is the prophylactic active immunization against Lyme disease in children and adults. Valneva’s program is the only active vaccined evelopment program for Lyme disease in the pharmaceutical industry. Valneva intends to initiate a Phase I trial in the US and Europe in 2016 with the primary objectives of evaluating safety and tolerability. Immunogenicity for six OspA serotypes will also be monitored for different dose groups and formulations. Pre-clinical results indicated that Valneva’s vaccine candidate can provide protection against the majority of Borrelia species…”

Excellent project hopefully ALL what they propose and the vaccine be a SUCCESS, but NOW…

1.) WHEN LYMErix was withdrawn the FDA PANEL concluded that the LIMErix vaccine was not associated with the production of ARTHRITIS. This is false. VAERS REPORT 322 cases of ARTHRALGIA associated with the vaccine. And the development of VACCINE-INDUCED ARTHRITIS in HLA patients HLA DR-4, now called LYME ARTHRITIS. 
2.) LYMErix was a SCIENTIFIC “SUCCESS” says valneva in his exposition. This is also FALSE. WHY DOES THE POPULATION REJECT IT? Because of the great side effects !!! Why did the patients wrote to the FDA PRAYING that LYMErix was removed from the market. ? SIMPLY, BECAUSE IT WAS A FAILURE. 
3.) WHY DID VALNEVA not mention the patients who were DISABLED FOR EVER by the LYMErix vaccine and the 229 DEATHS I REPORT THE SAME FDA. ? 
I’m going to tell you why VALNEVA “OMITTED” these data: THE ANSWER IS SIMPLE AND UNIQUE: 
The new vaccine VL15-101 that is being proposed for LYME DISEASE is based on the same immunological concept of LYMErix VACCINE OspA. Surface proteins of BORRELIA BURGORFERI. The rest is history. (see attached)

On the other hand, it is interesting that you know that in your immune system there is the Major Histocompatibility Complex (MHC) and its HLA (Histocompatibility Antigens) Molecules Class I A, B, and C, and CLASS II DR and DQ MOLECULES. This have been studied by geneticists For more than 30 years and numerous DERMATOLOGICAL and NON-DERMATOLOGICAL diseases have been associated with these antigens.
In the case of LYME DISEASE, HLA DR-4 antigen and HLA B-27 have been associated with ARTHRITIS, while other infectious diseases present in a certain person can “detonate” an HLA antigen to express itself and thereby Worsen a PRE-EXISTING illness, or express a NEW ILLNESS. 
The big question is this – Are HLA studies in the population affected by LYME DISEASE being done?  These studies were done before placing the LYMErix vaccine? They are currently being done with volunteers for the “NEW VACCINE VL15?”. 
As a tip I tell you that Australia did a study on 555 dogs looking for BORRELIA BURGDORFERI, and I came to the conclusion that in this area of ​​the planet there is no LYME disease. In Canada they did it in 2013-2014 and it was concluded that BORRELIOSIS is endemic in that country.
On the other hand, it is well known that LYME DISEASE that does not respond well to treatment, becomes CHRONIC and costs are high. AND ALL OF YOU KNOW THAT INSURANCE COMPANIES DO NOT WANT TO PAY. 
Then it is easier, to create a new expectation, A NEW VACCINE 15 YEARS AFTER THE FAILURE OF LYMErix, for two important facts:
Hopefully VALNEVA will do the proper science and not mislead anyone, and the FDA WILL NOT APPROVE THE VACCINE if the proper science is not done.  If it passes the tests WELCOME the new one.
Finally I say the following, VACCINE VL15 is in PHASE I, which means that are testing the SAFETY in people, if it overcomes this obstacle, it will come to Phase II, to prove how well it works PREVENTING LYME disease. Then Phase III, to test it in a broader population RANGE and at different doses.
Cost: about $3 billion. As a note, I tell you that 86% DO NOT PASS the TWO FINAL STAGES, AND 94% of drugs tested on ANIMALS do NOT pass HUMAN tests. So VL15 of valneva has a LONG ROAD to go.
And now I ask you? Are you willing to try a VACCINE while being totally healthy that could trigger in you ANY ILLNESS you would never otherwise suffer? 
Did you know that in your immunological composition are HISTOCOMPATIBILITY ANTIGENS, (HLA) that by a simple incidence can “TRIGGER” unknow disease?
We will be looking forward to this new project and as always I wish the BEST TO THIS COMPANY THAT TRIES TO DEVELOP a new LYMErix or VL15 for LYME disease.
In the references and attachments the facts …
1.) Immunogenetic Markers Definition in Latvian Patients with Lyme Borreliosis and Lyme Neuroborreliosis.
2.) Associations of HLA DR and DQ molecules with Lyme borreliosis in Latvian patients.
3.) The genospecies B. burgdorferi s.l., isolated from ticks and from neurological patients with suspected Lyme borreliosis.
4.) [Critical analysis of reference studies on aluminium-based adjuvants toxicokinetics].
5.) Human-leukocyte antigen class II genes in early-onset obsessive-compulsive disorder.
6.) Differential diagnoses of suspected Lyme borreliosis or post-Lyme-disease syndrome.
7.) HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations.
8.) Searching for Lyme borreliosis in Australia: results of a canine sentinel study.
9.) Canine infection with Borrelia burgdorferi, Dirofilaria immitis, Anaplasma spp. and Ehrlichia spp. In Canada, 2013-2014.
10.) Aluminum vaccine adjuvants: are they safe?
11.) Lyme Disease Testing by Large Commercial Laboratories in the United States 
1.) Immunogenetic Markers Definition in Latvian Patients with Lyme Borreliosis and Lyme Neuroborreliosis.
Kovalchuka L1, Cvetkova S2, Trofimova J3, Eglite J4, Gintere S5, Lucenko I6, Oczko-Grzesik B7, Viksna L8, Krumina A9,10.
Author information 
Institute of Food Safety, Animal Health and Environment BIOR, Riga LV-1076, Latvia.
Institute of Food Safety, Animal Health and Environment BIOR, Riga LV-1076, Latvia.
Institute of Food Safety, Animal Health and Environment BIOR, Riga LV-1076, Latvia.
Laboratory of Clinical Immunology and Immunogenetic, Riga Stradiņš University, Riga LV-1067, Latvia.
Department of Family Medicine, Riga Stradiņš University, Riga LV-1067, Latvia.
Centre for Disease Prevention and Control of Latvia, Riga LV-1005, Latvia.
Department of Infectious Diseases, Medical University of Silesia, 40-055 Katowice, Poland.
Department of Infectology and Dermatology, Riga Stradiņš University, Riga LV-1006, Latvia.
Institute of Food Safety, Animal Health and Environment BIOR, Riga LV-1076, Latvia.
Department of Infectology and Dermatology, Riga Stradiņš University, Riga LV-1006, Latvia. 
The aim of this study was to determine the human leukocyte antigen (HLA)-DRB1 alleles in two groups of patients in Latvia: patients with Lyme borreliosis and patients with Lyme neuroborreliosis. The study included 216 patients with Lyme borreliosis, 29 patients with Lyme neuroborreliosis and 282 control persons. All surveyed persons were residents of Latvia. The HLA-DR genotyping was performed by polymerase chain reaction- sequence specific primer (PCR-SSP). The predisposition to the Lyme borreliosis is associated with the HLA-DRB1*07, -DRB1*17(03), -DRB1*04, -DRB1*15(02) alleles. The allele -DRB1*11(05), -DRB1*14(06) and -DRB1*13(06) were significantly more frequent in controls. In-group with Lyme neuroborreliosis differences were found for the -DRB1*07 and -DRB1*04 alleles, but only HLA-DRB1*07 allele was statistically significant after Bonferroni correction and associated with Lyme neuroborreliosis in Latvian patients.
2.) Associations of HLA DR and DQ molecules with Lyme borreliosis in Latvian patients.
Kovalchuka L1, Eglite J, Lucenko I, Zalite M, Viksna L, Krumiņa A.
Author information 
Riga Stradiņš University, Clinical Immunology and Immunogenetic laboratory, Kronvalda Str 9, Riga, Latvia. 
Many autoimmune diseases are associated with variants of HLA genes such as those encoding the MHC complex. This correlation is not absolute, but may help in understanding of the molecular mechanism of disease. The purpose of this study was to determine HLA-DR,-DQ alleles in Latvian patients with Lyme borreliosis and control (healthy) persons. Case patients and control subjects were similar in age, gender and ethnic heritage and differed only as regards the presence of Borrelia burgdorferi infection. The study included 25 patients with clinical stage – erythema migrans and 30 control (healthy) persons. HLA genotyping was performed by PCR with sequence-specific primers.
The results show difference in HLA-DRB1 alleles distribution between patients and control subjects. The frequencies of HLA-DRB1 *04 (OR 11.24; p < 0.007) and HLA-DRB1 *17 (03) (OR 8.05; p < 0.033) were increased in the Lyme disease patients. And the frequency of allele DRB1*13 (OR 0.12; p < 0.017) was lower in Borreliosis patients and higher in control group. But, significant differences in frequencies of HLA-DQ alleles we did not detect.
HLA predisposition to Lyme borreliosis appears not to be limited to HLA molecules, but some HLA-DR alleles also have a significant influence, and, may have implications in our understanding of pathogenesis of this disease. In particular, HLA-DRB1*04 and DRB1 *17 (03) may contribute to the Lyme borreliosis development in Latvian population.
3.) The genospecies B. burgdorferi s.l., isolated from ticks and from neurological patients with suspected Lyme borreliosis.
Neuro Endocrinol Lett. 2011;32(4):491-5. 
Bazovska S1, Durovska J, Derdakova M, Taragelova V, Pancak J, Zaborska M, Traubner P.
Author information 
Institute of Epidemiology, Comenius University, Bratislava, Slovakia. 
Lyme borreliosis (LB) is the most disseminated tick-borne disease in the Northern hemisphere, and infestation with ticks is one of the essential factors influencing transmission of the disease to humans. This work intends to compare the occurrence of borrelia circulating in indigenous ticks and in patients suffering from neurological diseases.
The total of 660 nymphs and 567 adult ticks from the Bratislava and Košice areas was examined over the years 2001-2004, and the cerebrospinal fluid (CSF) of 82 neurological patients suffering from suspected Lyme borreliosis infection was investigated in the 2007-2009 period, using the polymerase chain reaction method (PCR).
PCR investigation proved presence of borrelia in 23.3% of the total 1227 ticks; of these, co-infection was found in 2.7% of all ticks. Borrelia garinii (9.9%) and B. valaisaina (9.2%) were the prevalent types. PCR investigation of the CSF samples of 32 patients with clinically diagnosed Lyme borreliosis showed the presence of B. burgdorferi s.l. in 17 cases. Positive results were found also in patients with unclear or different diagnoses. In cases where the genospecies could be identified, B. garinii was most frequently found (8x), followed with B. burgdorferi s.s. (4×) and B. afzelii (3×).
The high infestation level of ticks with borrelia, mainly with B. garinii which is the most-often documented borrelia species identified in neurological patients, is indicative of a high risk of this contamination in Slovakia. B. garinii were found also in our neuroborreliosis patients, whereas their proof in the CSF of patients with suspected neuroborreliosis or with a different clinical diagnosis pointed upon their persistence after an infectious experience. However, knowledge of not only the genospecies but also of the genotypes capable of eliciting an invasive disorder would be necessary for better clarification of the relationship between borrelia and their peccant capacity. Identification of the invasive borrelia types circulating in nature, and clarification of the vector vs. human infection incidence relationship is of importance from the aspect of detailed knowledge of the epidemiology of this disease.
4.) [Critical analysis of reference studies on aluminium-based adjuvants toxicokinetics].
Ann Pharm Fr. 2017 May 30. pii: S0003-4509(17)30033-0. doi: 10.1016/j.pharma.2017.04.004. [Epub ahead of print] 
[Article in French]
Masson JD1, Crépeaux G2, Authier FJ1, Exley C3, Gherardi RK4.
Author information 
Inserm U955 E10, centre expert de pathologie neuromusculaire, « Biologie du système neuromusculaire », hôpital Henri-Mondor, faculté de médecine, université Paris-Est-Créteil, 94010 Créteil, France.
Inserm U955 E10, centre expert de pathologie neuromusculaire, « Biologie du système neuromusculaire », hôpital Henri-Mondor, faculté de médecine, université Paris-Est-Créteil, 94010 Créteil, France; École nationale vétérinaire d’Alfort, 7, avenue du Général-de-Gaulle, 94700 Maisons-Alfort, France.
Aluminium and Silicon Research Group, The Birchall Centre, Lennard-Jones Laboratories, Keele University, ST5 5BG, Staffordshire, Royaume-Uni.
Inserm U955 E10, centre expert de pathologie neuromusculaire, « Biologie du système neuromusculaire », hôpital Henri-Mondor, faculté de médecine, université Paris-Est-Créteil, 94010 Créteil, France. Electronic address: 
We reviewed the three reference toxicokinetic studies commonly used to suggest innocuity of aluminum (Al)-based adjuvants. A single experimental study was carried out using isotopic 26Al (Flarend et al., 1997). This study ignored adjuvant cell capture. It was conducted over a short period of time (28 days) and used only two rabbits per adjuvant. At the endpoint, Al retention was 78% for aluminum phosphate and 94% for aluminum hydroxide, both results being incompatible with quick elimination of vaccine-derived Al in urines. Tissue distribution analysis omitted three important retention sites: the injected muscle, the draining lymph node and bone. Two theoretical studies have evaluated the potential risk of vaccine Al in infants, by reference to the oral Minimal Risk Level (MRL) extrapolated from animal studies. Keith et al., 2002 used a too high MRL (2mg/kg/d), an erroneous model of 100% immediate absorption of vaccine Al, and did not consider renal and blood-brain barrier immaturity. Mitkus et al. (2011) only considered absorbed Al, with erroneous calculations of absorption duration. They ignored particulate Al captured by immune cells, which play a role in systemic diffusion and the neuro-inflammatory potential of the adjuvant. MRL they used was both inappropriate (oral Al vs injected adjuvant) and far too high (1mg/kg/d) with regard to experimental studies of Al-induced memory and behavioral changes. Both paucity and serious weaknesses of these studies strongly suggest that novel experimental studies of Al adjuvants toxicokinetics should be performed on the long-term, including post-natal and adult exposures, to ensure innocuity and restore population confidence in Al-containing vaccines.
5.) Human-leukocyte antigen class II genes in early-onset obsessive-compulsive disorder.
Rodriguez N1,2,3, Morer A2,3,4, González-Navarro EA3,5, Gassó P1,3, Boloc D1, Serra-Pagès C3,5,6, Lafuente A1,2,3, Lazaro L2,3,4,7, Mas S1,2,3.
Author information 
a Dept. Anatomic Pathology, Pharmacology and Microbiology , University of Barcelona , Barcelona , Spain.
b Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM) , Barcelona , Spain.
c Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) , Barcelona , Spain.
d Department of Child and Adolescent Psychiatry and Psychology, Institute of Neurosciences , Hospital Clinic de Barcelona , Barcelona , Spain.
e Immunology Service , Centre de Diagnostic Biomèdic, Hospital Clínic Dept , Barcelona , Spain.
f Dept. Biomedicine , University of Barcelona , Barcelona , Spain.
g Psychiatry and Clinical Psychobiology , University of Barcelona , Barcelona , Spain. 
The exact aetiology of obsessive-compulsive disorder (OCD) is unknown, although there is evidence to suggest a gene-environment interaction model. Several lines of evidence support a possible role of the immune system in this model.
The present study explores the allele variability in HLA genes of class II (HLA-DRB1, HLA-DQB1) in a sample of 144 early-onset OCD compared with reference samples of general population in the same geographical area.
None of the 39 alleles identified (allele frequency >1%) showed significant differences between OCD and reference populations. Pooling the different alleles that comprised HLA-DR4 (including DRB1*04:01, DRB1*04:04 and DRB1*04:05 alleles) we observed a significantly higher frequency (X21 = 5.53, P = 0.018; OR = 1.64, 95% CI 1.08-2.48) of these alleles in the early-onset OCD sample (10.8%) than in the reference population (6.8%).
Taking into account the role of HLA class II genes in the central nervous system, the results presented here support a role of the immune system in the pathophysiological model of OCD.
6.) Differential diagnoses of suspected Lyme borreliosis or post-Lyme-disease syndrome.
Eur J Clin Microbiol Infect Dis. 2007 Sep;26(9):611-7. 
Seidel MF1, Domene AB, Vetter H.
Author information
The symptoms of Lyme borreliosis are similar to those of a variety of autoimmune musculoskeletal diseases. Persistence of complaints is frequently interpreted as unsuccessful antibiotic treatment of Borrelia-associated infections. However, such refractory cases are rare, and re-evaluation of differential diagnoses helps to avoid the substantial risk of long-term antibiotic therapy. In this study, we analyzed patients who presented to our rheumatology unit with previous suspected or diagnosed Lyme borreliosis. Eighty-six patients from a 3.5-year period were evaluated. The mean age of patients was 49.2 +/- 17.2 years; 60% (n = 52) reported a tick bite and 33% (n = 28) an erythema. Forty-seven percent (n = 39) had positive enzyme-linked immunoassay results and Western blots (Mikrogen, Martinsried, Germany). All but 12 patients had already received antibiotic treatment previously. Nine percent (n = 8) had ongoing or recent Lyme borreliosis. Twenty-nine percent (n = 25) showed clinical symptoms and radiographic changes compatible with degenerative disorders of the cervical and/or lumbar spine. These patients were significantly older when compared to the other patients (59.3 +/- 13.7 years vs 46.1 +/- 17.2 years, p = 0.001). Seventeen percent (n = 16) had arthropathies related to psoriasis or rheumatoid arthritis. Twelve percent (n = 10) were positive for the HLA B27 antigen. Other diseases were less frequent. Six patients (7%) could not be diagnosed conclusively, and four of these patients had negative Borrelia immunoassay results. In conclusion, Borrelia-associated diseases were rare in this study. Differential diagnoses helped to initiate a successful disease-specific therapeutic strategy.
7.) HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations.
Clin Microbiol Rev. 2004 Apr;17(2):348-69. 
Colmegna I1, Cuchacovich R, Espinoza LR.
Author information 
Section of Rheumatology, Department of Medicine, LSU Health Science Center, New Orleans, Louisiana 70112, USA. 
Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, non-culturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease. 
Reactive arthritis (ReA) is defined as a sterile synovitis developing after a distant infection, usually in the genitourinary or gastrointestinal tract. The detection of microbial components (microbial DNA and RNA) in the joints of patients with ReA has led to the reconsideration of this definition (59). Currently, ReA is better defined as an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. A classification into HLA-B27-associated and nonassociated forms has also been proposed. Post-streptococcal, Lyme, and viral arthritis are HLA-B27 nonassociated and should be described as distinct entities under the general heading of “infection-related arthritides.” 
This article focuses on HLA-B27-associated ReA. This form of ReA belongs to the group of spondyloarthropathies (SpA), is triggered by bacteria (which enter the body through the mucosal surfaces) from the genera Campylobacter, Chlamydia, Salmonella, Shigella, and Yersinia, and is clinically associated with oligoarthritis of the lower limbs and sometimes with urethritis and conjunctivitis.
8.) Searching for Lyme borreliosis in Australia: results of a canine sentinel study.
Parasit Vectors. 2017 Mar 13;10(1):114. doi: 10.1186/s13071-017-2058-z. 
Irwin PJ1,2, Robertson ID3, Westman ME4, Perkins M5, Straubinger RK6.
Author information 
Vector and Water-Borne Pathogen Research Group, School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, 6150, Australia.
College of Veterinary Medicine, School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, 6150, Australia.
College of Veterinary Medicine, School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, 6150, Australia.
Sydney School of Veterinary Science, University of Sydney, Sydney, New South Wales, 2006, Australia.
Pymble Veterinary Clinic, Philip Mall, Kendall Street, West Pymble, New South Wales, 2073, Australia.
Department of Infectious Diseases and Zoonoses, Bacteriology and Mycology, Ludwig-Maximilians-University Munich, 80539, Munich, Germany. 
Lyme borreliosis is a common tick-borne disease of the northern hemisphere that is caused by bacterial spirochaetes of the Borrelia burgdorferi (sensu lato) (Bbsl) complex. To date, there has been no convincing evidence for locally-acquired Lyme borreliosis on the Australian continent and there is currently a national debate concerning the nature and distributions of zoonotic tick-transmitted infectious disease in Australia. In studies conducted in Europe and the United States, dogs have been used as sentinels for tick-associated illness in people since they readily contact ticks that may harbour zoonotic pathogens. Applying this principle, we used a combination of serological assays to test dogs living in tick ‘hot spots’ and exposed to the Australian paralysis tick, Ixodes holocyclus, for evidence of exposure to B. burgdorferi (s.l.) antigens and other vector-borne pathogens.
Altogether, 555 dogs from four demographic groups were recruited into this study. One dog had evidence of exposure to Anaplasma spp. but no other dog was positive in screening tests. A total of 122 dogs (22.0%) had a kinetic ELISA (KELA) unit value > 100, and one dog with a high titre (399.9 KELA units) had been vaccinated against B. burgdorferi (sensu stricto) before travelling to Australia. Older dogs and those with a history of tick paralysis were significantly more likely to have a KELA unit value > 100. Line immunoassay analysis revealed moderate-to-weak (equivocal) bands in 27 (4.9%) dogs.
Except for a single dog presumed to have been exposed to Anaplasma platys, infection with Anaplasma spp. B. burgdorferi (s.l.), Ehrlichia spp., and Dirofilaria immitis, was not detected in the cohort of Australian dogs evaluated in this study. These results provide further evidence that Lyme borreliosis does not exist in Australia but that cross-reacting antibodies (false positive results) are common and may be caused by the transmission of other tick-associated organisms.
9.) Canine infection with Borrelia burgdorferi, Dirofilaria immitis, Anaplasma spp. and Ehrlichia spp. In Canada, 2013-2014.
Parasit Vectors. 2017 May 19;10(1):244. doi: 10.1186/s13071-017-2184-7. 
Herrin BH1, Peregrine AS2, Goring J3, Beall MJ3, Little SE4.
Author information 
Department of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, USA.
Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
IDEXX Laboratories, Inc, Westbrook, ME, USA.
Department of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, USA. 
Canine test results generated by veterinarians throughout Canada from 2013-2014 were evaluated to assess the geographical distribution of canine infection with Borrelia burgdorferi, Dirofilaria immitis, Ehrlichia spp., and Anaplasma spp.
The percent positive test results of 115,636 SNAP® 4Dx® Plus tests from dogs tested were collated by province and municipality to determine the distribution of these vector-borne infections in Canada.
A total of 2,844/115,636 (2.5%) dogs tested positive for antibody to B. burgdorferi. In contrast, positive test results for D. immitis antigen and antibodies to Ehrlichia spp. and Anaplasma spp. were low, with less than 0.5% of dogs testing positive for any one of these three agents nationwide. Provincial seroprevalence for antibodies to B. burgdorferi ranged from 0.5% (Saskatchewan)-15.7% (Nova Scotia); the areas of highest percent positive test results were in proximity to regions in the USA considered endemic for Lyme borreliosis, including Nova Scotia (15.7%) and Eastern Ontario (5.1%). These high endemic foci, which had significantly higher percent positive test results than the rest of the nation (P < 0.0001), were surrounded by areas of moderate to low seroprevalence in New Brunswick (3.7%), Quebec (2.8%), and the rest of Ontario (0.9%), as well as northward and westward through Manitoba (2.4%) and Saskatchewan (0.5%). Insufficient results were available from the westernmost provinces, including Alberta and British Columbia, to allow analysis.
10.) Aluminum vaccine adjuvants: are they safe?
Curr Med Chem. 2011;18(17):2630-7. 
Tomljenovic L1, Shaw CA.
Author information 
Neural Dynamics Research Group, Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, BC, V5Z 1L8, Canada. 
Aluminum is an experimentally demonstrated neurotoxin and the most commonly used vaccine adjuvant. Despite almost 90 years of widespread use of aluminum adjuvants, medical science’s understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. In spite of this, the notion that aluminum in vaccines is safe appears to be widely accepted. Experimental research, however, clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. In particular, aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences. In our opinion, the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community. We hope that the present paper will provide a framework for a much needed and long overdue assessment of this highly contentious medical issue.
11.) Lyme Disease Testing by Large Commercial Laboratories in the United States 
Alison F. Hinckley Neeta P. Connally James I. Meek Barbara J. Johnson Melissa M. Kemperman Katherine A. Feldman Jennifer L. White Paul S. Mead
Clin Infect Dis (2014) 59 (5): 676-681. 
Published: 30 May 2014 
Large commercial laboratories in the United States were surveyed to determine Lyme disease testing frequency, practices, and results. Approximately 3.4 million tests were conducted in 2008; 62% in accordance with recommendations. We estimate that 288 000 infections occurred among 2.4 million patients from whom samples were submitted.
Background. Laboratory testing is helpful when evaluating patients with suspected Lyme disease (LD). A 2-tiered antibody testing approach is recommended, but single-tier and nonvalidated tests are also used. We conducted a survey of large commercial laboratories in the United States to assess laboratory practices. We used these data to estimate the cost of testing and number of infections among patients from whom specimens were submitted.
Methods. Large commercial laboratories were asked to report the type and volume of testing conducted nationwide in 2008, as well as the percentage of positive tests for 4 LD-endemic states. The total direct cost of testing was calculated for each test type. These data and test-specific performance parameters available in published literature were used to estimate the number of infections among source patients.
Results. Seven participating laboratories performed approximately 3.4 million LD tests on approximately 2.4 million specimens nationwide at an estimated cost of $492 million. Two-tiered testing accounted for at least 62% of assays performed; alternative testing accounted for <3% of assays. The estimated frequency of infection among patients from whom specimens were submitted ranged from 10% to 18.5%. Applied to the total numbers of specimens, this yielded an estimated 240 000 to 444 000 infected source patients in 2008.
Discussion. LD testing is common and costly, with most testing in accordance with diagnostic recommendations. These results highlight the importance of considering clinical and exposure history when interpreting laboratory results for diagnostic and surveillance purposes.


For more:   So …in 1994, the CDC hosted a consensus conference in Dearborn, MI, along with a dozen labs across the country and together they falsified the very definition of Lyme disease by eliminating the neurological, immunosuppressive type which account for 85% of the cases.

If they conveniently ‘determined’ that the 85% group – those with an immunosuppression neurological outcome––simply did NOT exist, then they could claim that their vaccine was 85% effective. With no immunosuppressive, neurological disease to find, then the vaccine would be a hit with the remaining 15% who presented with an arthritic, bad-knee type only. A brilliant marketing scheme at the expense of millions worldwide for the years to come.
You see, you CANNOT create a vaccine for an OspA fungal antigen — the TRUE definition of chronic Lyme. It can’t be done. And the OspA vaccination known as LYMErix caused the same disease from a syringe as it does when you get Lyme disease from a tick bite. LYMErix victim’s immune systems were destroyed by the vaccine because OspA is an endotoxin that causes immunosuppression and subsequent severe neurologic multi-system disease.
So by narrowing the definition and by claiming that only one type of the disease (the bad knee arthritic type) exists, then they could sell a vaccine. Not only that. They were also able to profit by limiting the number of labs that were sanctioned and thereby cornering the market on the patents of a variety of tick borne diseases.
THE FIRST LYME VACCINE WAS A COMPLETE BUST.  In a vile cesspool of conflicts of interest are university patent holders, drug companies, and the FDA itself as another patent holder. It generated 40 million dollars before it was yanked. (2008, Drymon) One doctor stated that 21 patients developed severe arthritis after receiving the LYMERIX vaccine. The biological mechanism hypothesis was that the outer surface protein A (OspA), which was the antigenic component of the LYMErix vaccine, induced autoimmunity in genetically susceptible individuals, including high levels of autoantibody to OspA in their synovial fluid.

Dr. Stricker states:

Another Lyme OspA Vaccine Whitewash
The meta-analysis by Zhao and colleagues comes to the conclusion that “the OspA vaccine against Lyme disease is safe and its immunogenicity and efficacy have been verified.” The authors arrive at this sunny conclusion by excluding 99.6% of published articles that demonstrate potential problems with the OspA vaccine.Furthermore, the authors ignore peer-reviewed studies, FDA regulatory meetings and legal proceedings that point to major problems with OspA vaccine safety (1-3). This whitewash bodes ill for future Lyme vaccine candidates because it fosters disregard for vaccine safety among Lyme vaccine manufacturers and mistrust among potential Lyme vaccinees.

Also, I find it highly intriguing that the push here, and always, is for a vaccine; not a cure, not helping patients with pain, not making care accessible and affordable. Just in creating a new cash-cow for a select few.  Patients be damned.


LD & The Brain – Podcast With Dr. Bransfield

Episode 23: Lyme Disease and the Brain

Cindy Kennedy, FNP, is joined by Dr. Robert C. Bransfield, M.D., F.A.P.A., who discusses Lyme disease and the brain, including the connection between Lyme disease and mental health and how Lyme disease and co-infections can cause cognitive impairments, sleep disorders and various psychiatric issues.

Dr. Bransfield is a graduate of Rutgers College and the George Washington University School of Medicine. He completed his psychiatric residency training at Sheppard and Enoch Pratt Hospital. He is board certified by the American Board of Psychiatry and Neurology in Psychiatry. 

Dr. Bransfield’s primary activity is office-based private practice of psychiatry with an emphasis upon treatment resistant cases. In addition, Dr. Bransfield is the Associate Director of Psychiatry and the Chairman of Quality Assurance at Riverview Medical Center in Red Bank, N.J.

He has held teaching appointments at Hahnemann Medical College and Eastern Virginia Medical School. He has taught in many settings to physicians, mental health professionals and the public. He has performed research, and has a particular interest in psychopharmacology, a unified theory of mental health and illness, the link between microbes and mental illness, Lyme and other tick-borne disease, violence, and the link between microbes and violence.

Dr Bransfield has authored and co-authored a number of publications in peer-reviewed literature, other medical publications and books. He has held a number of administrative positions for various organizations involved with a number of health, mental health and community related activities.

Dr Bransfield has been active in political advocacy on a national, state and local level. He has appeared on network and regional television, radio and various publications.

Transcript of Episode 23: Lyme Disease and the Brain

Cindy K.: This is Cindy Kennedy your host and we are on the Living with Lyme today. We have the great honor of having Dr. Robert Bransfield with us. He is well versed and considered an expert in the area of Lyme and other tickborne diseases and the treatment of neuropsychiatric symptoms. He’s active in political advocacy on national state and local levels. He’s also been an author and a speaker. He has notable publications in peer-reviewed literature. We’ve had a lot of technical issues today but we finally have him and I’d like to welcome Dr. Bransfield. How are you today?

Robert B.: Good Cindy. It’s good to be here.

Cindy K.: Oh it is. It is. I’m so thankful because your expertise goes beyond the scope of anything I can imagine. I’m sure the information that you and I are going to talk about are going to be very, very helpful to a lot of people. So, my question to you is, we know that Lyme is certainly underdiagnosed and undertreated. I think for most healthcare professionals that a psychiatric presentation is highly unlikely and they wouldn’t consider Lyme and all the symptoms that go along with it. Can you give your experience on that?

Robert B.: Yes. What happens is many of the doctors who have capability, experience, credentials for treating early infectious disease invariably have very little training in psychiatry. So, you may find that patients go to infectious disease doctors, rheumatologists and they haven’t had much current experience with psychiatry. When I ask them, “What’s your training in psychiatry?” They may say that 40 years ago they did a one-month rotation in a state psychiatric hospital and that might be the extent of their psychiatric training. So, they have difficulty seeing the connection between the physiological process that occurs that impacts the brain that then results in psychiatric symptoms.

Cindy K.: You know Dr.-

Robert B.: You can tell their training may go back to the old Freudian theories and it’s hard for them to understand the physical basis to the mental symptoms that we see.

Cindy K.: Dr. Bransfield, hold on one second. Don’t speak so close to the phone because it’s hissing a little bit. So, I’m sorry. I’m going to go back to the point where I asked you, what is your experience with these doctors not understanding that there can be psychiatric presentations?

Robert B.: I think many doctors just lack the training in understanding the physiology as how mental illnesses are caused by brain inflammation. Many doctors who treat earlier cases of Lyme disease have knowledge in infectious disease but they don’t have knowledge or extensive knowledge in psychiatry. Some have only had maybe one-month rotation decades ago when they were in medical school and have not kept current with current physiology, understanding as how brain processes can cause mental symptoms. So, I think that’s a big problem is the disparity, the gap between infectious disease in psychiatry.

Cindy K.: Is there any certain type of patient that comes to you with particular psych issues that would prompt you to immediately think “Geez, could this be Lyme?”?

Robert B.: Yes. The more common cases often it’s progressive. So, the mental symptoms keep getting worse and a particularly common case would be someone who is partially treated for Lyme disease. The partial treatment may be enough to help some of the … or major part of musculoskeletal symptoms, but not enough to help the cognitive and the neuropsychiatric and some of the neurological symptoms. So, that’s the case. It can go under the radar for diagnosis since it’s not your migratory arthralgia, your type of presentation that most people would recognize Lyme disease.
So, this typical case is someone who’s symptoms keep getting worse with time and you give a treatment that works for a while and then they keep getting worse. It’s a combination. It’s a multisystem illness and you have to look at all the different ways it presents and every patient is all but different but you see invariably fatigue, multiple cognitive impairments, multiple psychiatric symptoms, anxiety, depression, irritability and sleep disorders and then neurological symptoms, neuropathy. So, it spans almost every system in the body.

Cindy K.: Do certain co-infections exaggerate psychiatric symptoms or would you see a particular psychiatric symptoms more often with say babesia?

Robert B.: So, invariably when we look at the more severe psychiatric cases we find co-infections. It may be that when someone has Lyme alone maybe that’s not as bad. When co-infections are present, it’s not an additive effect. It’s an interactive effect. So, when you add to infections, they interact in a way that can magnify the degree of severity. So, we babesia, bartonella, mycoplasma and these are opportunistic viruses. Probably other things that we aren’t really testing for chlamydia, rickettsia, ehrlichia, the more severe cases often have multiple co-infections.

Cindy K.: Now you said I’m thinking to myself and we had a discussion a little earlier about someone that I know having an onset which looks to be Parkinsonian and of course that goes along with when your body is not really … it’s breaking down in some sorts that you get depression. So, when you’re talking out psychiatric issues, is it something that’s kind of insidious that leads you? Is there a rapid onset of say dementia that would trigger some sort of a concern because maybe it’s not in the family, maybe again it wasn’t something that … it just came up very quickly. Is that something you’d see?

Robert B.: Sometimes. I think the more common case seems to be someone who has infection more in the body there’s an immune reaction. Rather than adaptive immunity and the infection’s gone, you see with these infections persistent inflammation and autoimmunity and disease progression. Now there are some cases where … these are the cases I think where there’s infection in the brain rather than infection in the body provoking the immune system which causes mental symptoms. The cases where there’s clear infection in the brain, those can appear as a more rapidly progressive dementia case. We used to call these pre-senile dementia but this can be a relatively young person and it’s a very rapid downhill course even with a fair amount of antibiotics that may just slow it down. These are very difficult cases.
Fortunately, they’re the minority but they’re very tragic when we see them and invariably on an autopsy then you can find borrelia in the central nervous system, but your average run-of-the-mill cases more rather than neuroborreliosis more Lyme encephalopathy where we have it in the body and it can affect the brain. So, you don’t have to have spirochetes inside the brain to get mental symptoms from Lyme disease. You can have it in the body and has that immune effects and that orders neural functioning because the cytokines and certain antigens from the infection can cause the blood brain barrier and cause mental symptoms. That’s why it can be episodic. Someone can be good in the morning and then several hours later be very impaired.

Cindy K.: I understand that oral antibiotics is not a great way to treat complications that are arising in the brain. It typically doesn’t cross the blood brain barrier. That you need to use more IV or possibly intramuscular injections. Is that true?

Robert B.: Right. If it’s actually in the brain, that might be true although it’s more an issue of how high a blood level you can get with antibiotics. If someone’s GI tract tolerates it, then you may be able to do it with orals and it might be effective. I think you do see more use of orals proportionally now than used to be the case whereas before in the earlier era of the Lyme epidemic, people would start out more with IV. One hesitation about that is if you start with a very aggressive antibiotic treatment, you might get a neuropsychiatric Herxheimer reaction where someone could have an exacerbation of their neuropsychiatric including suicidality. That could provoke a suicide attempt. So, I find it’s often better to gradually ramp up the treatment so that there isn’t too much of a Herxheimer reaction that could be destructive to the patient.

Cindy K.: This is an interesting question and I don’t have an answer. If you’re bitten by a tick that’s infected and it’s on the upper portion of your body, say you found it in your scalp versus something on a lower limb behind your knee. Does that trigger more neurologic per se?

Robert B.: Yes.

Cindy K.: It does.

Robert B.: Yes. There was one study done where they looked at the different quadrants of the body, because some of it’s dissemination through the blood but some of it’s local spread. In part this is why children may have more severe … one of the reasons why children may have more severe symptoms is because their … what happen is a tick would first get on the lower part of the body, work their way up until there’s some constriction. Then they would attach there. So, children are closer to the ground or their brains are closer to the ground than adult. There may be a three-foot trip instead of a six-foot trip to get up the length of an adult. So, when the ticks are attached, more in the head and neck region and that’s a common place where they are attached. You see that in deer also. They could be in the hairline, above the hairline. It does seem they do have more of the CNS symptoms when the attachment is closer to the brain.

Cindy K.: What type of neuro symptoms do children have versus adults? Is there any difference?

Robert B.: Yes. Well, one difference can be they invariably don’t have a reference point of what it’s like to not have symptoms. They don’t know what healthy is. So, if you’re an adult and at the age of 30 you get an infection, you know what you were like before the date of that infection then you may struggle to try to function at the level that you used to be at. So, you know what should be but a child who is developing doesn’t have that reference point. So, that’s a major problem. You invariably see a lot of tantrums, irritability, low frustration tolerance. It can be like behavior problems, obsessiveness, aggressive outbursts, difficulty with school. Some of it, it can look somewhat like attention deficit disorder but it qualitatively is different. There is a difference between Lyme and attention deficit disorder although some of the symptoms overlap.

Cindy K.: I did read an interesting story about a young boy who was very obsessive about being on his bicycle. It just came on very quickly. If he wasn’t eating in school or sleeping, he had to be on his bicycle. They were saying this child is obsessive compulsive. That’s all it is and the mom wouldn’t settle for that. It went on and went on. One doctor finally laid out all the paperwork, went through with a fine tooth comb and did find that he had a tick bite sometime prior and wasn’t treated. When they tested him, he was Lyme positive. They treated him and that compulsion to be on the bike just went away. I find that-

Robert B.: That was the famous case of bicycle boy with Andy Pachner. That goes back 30 years ago.

Cindy K.: Oh it does.

Robert B.: So, that case as a 30-year-old case and that was one of the earlier recognitions of the psychiatric manifestations of Lyme disease. Then that was also published in the magazine in Washington DC and that was included in the case histories. It was around ’87 or ’88 that that was published. So, that’s a 30-year-old case. So, this isn’t anything new to connect the psychiatric symptoms with Lyme disease. This has been around for a while and there’s been expanding recognition with many journal articles. Yet even with that, it’s … so for the rank-and-file doctor to catch on and see that connection.

Cindy K.: That might be a very hard one. Let’s talk about the nitty-gritty, because the vast majority of the people that are suffering are suffering with certain types of problems. I think we need to hear about why these problems are occurring. I’m going to start first with brain fog, that horrible inability to process things, to feel like you’re on your game. It commonly goes with that horrific fatigue. Where is that coming from?

Robert B.: Well bran fog is supported what we call sickness syndrome. Sickness syndrome, you could replicate it and it’s replicated when people have interferon treatment or when they get the cold or the flu and their inflammatory … part of their immune system is activated. So, lupus patients call it lupus fog. Fibro patients call it fibro fog. That fog, the best way to compare it is go take 100 mg of Benadryl in the morning and then go back your daily activities and see how you feel. So, it’s that fog that’s a thought like your brain is sluggish. Now you can see why it’s called the terrible triad. Terrible triad can be nonrestorative sleep, cognitive impairment and fatigue. So, the three can go together.
Now brain fog can be akin to like mental fatigue. Mental fatigue and physical fatigue have some similarities where there’s a sluggishness, the slowness and fatigue in the body is a lack of physical energy unrestored by rest. Compared to exhaustion, exhaustion you ran a marathon and now you’re exhausted because you expanded some energy whereas fatigue you wake up after 12 hours of sleep and you feel like you ran a marathon even though you did not. So, it’s that both cases that lack of physical energy. It’s a very frustrating symptom.
I think overall it’s very hard. People get the symptoms and they wish they didn’t have them. They can’t explain them. They can’t understand them. Their family can’t understand it. Just stop it and everybody wishes it would work that way. Then their doctors don’t understand it. Your insurance company doesn’t want to understand it. It’s baffling but there is a very clear explanation for it. It takes more complicated model and then we can understand it very clearly.

Cindy K.: You can’t just draw blood. See, that’s the thing. You can’t just draw blood that shows this particular issue, can you?

Robert B.: Well, this is a complex disease. You can’t use a simple diagnostic model to explain a complex disease. You have to use a complex model to explain a complex disease. Now it’s not that simple that you could just do one simple test. The reality if you look at the history of medicine, diseases that are simple have all been discovered, well understood well explained. What is left that is still at the leading edge of discovery in medicine are the more complex diseases that require more complex formula. If people keep using the simple “Let’s just do a blood test. If it’s positive, you have it. If it’s negative, you don’t.”
As long as you approach a complex disease in that way, you’ll be going around in circles never understand it, never solve it. You have to shift to a different model and recognizing the full complexity, there may be multiple interactive co-infections, multiple immune reactions and multiple manifestations. Now probably looking forward, there’s more in the way of gene testing and particularly these more sophisticated DNA testing for microbes. As that gradually gets online, I think that we can understand this much better. How you have a mix of infectious agents and then once this disease takes hold, orders what genes are turned on and turn off in our body. Often you’re looking at immune system genes. Then that correlates with the symptoms. That’s the model you need. Anything short of that is futility.

Cindy K.: Right. The other things that people experience are confusion or memory or word find issues. That lack of ability to concentrate or you’re reading something and you’re reading it five times and you still can’t remember. Is that also a process of that inflammation that happens as your body is trying to recover itself from an infection?

Robert B.: Yes. I think you can break it down in a couple areas. One is executive functioning and another is slow processing. Maybe slow processing … I’ll talk about that first. It’s easier to understand. Now think of a computer that has a slow processor. Invariably that’s a white line is more of a white matter dysfunction in the brain. When you do a MRI you see white matter hyperintensities. You see changes with the SPECT scan.

Cindy K.: What does that mean?

Robert B.: So, white matter is more the inside of the brain that has to do with processing. It is making the connections whereas something like Alzheimer’s is more of a gray matter disease where memory content is lost. So, if someone doesn’t remember the thing grandchildren that’s more a gray matter disease, but slowness of processing is white matter. So, invariably one way to compare it is in a Peanuts cartoon where when the adults are talking it’s wah, wah, wah, wah and the person is sitting there and they hear the words but they’re not digesting the content. So, it’s slow processing going in and going out, both. So, if it’s slow that helps.
Often a person can keep up with the conversation. So, like in a lecture hall in school, they’re not able to keep pace and digest the content. They can’t process it fast enough. Think of it like an assembly line. So, that’s going in but also going out. On going out, you can see that because a person’s struggling with word finding problems. You can see how they’re groping to correct, that they’re trying to solve. That type of thing. That’s what you’re seeing.

Cindy K.: [inaudible 00:22:37] I got nervous there. I see that you were trying to replicate what [crosstalk 00:22:42].

Robert B.: That’s why it works. So, it’s obvious and also if you explain something and you talk too fast, a person will just sit there with a blank expression on their face. You can see that they’re not really grasping what they’re saying. They need that slowness and-

Cindy K.: Is that because of inflammation though or do we not know?

Robert B.: [crosstalk 00:23:11] exactly but somehow it’s the connections are slow. Probably invariably inflammation is contributing to that. I first ran into that. I worked in a mental health clinic in North Carolina and there were these loggers that were there. I think looking back a lot of them had Lyme disease. It was a low-budget clinic and the consultation rooms are very small. You’d be in a tiny consultation room looking at someone maybe a foot or two in front of you and you’d say to them, “How are you doing today?” Then they’d look with a blank expression and say, “Who? Me?” A lot of them did this. It was very puzzling why they did that.
We tried to explain it and at the time we never could, but looking back I think the lot had Lyme disease. By saying, “Who? Me?” they were buying time to collect their thoughts. They couldn’t just answer because they weren’t processing fast enough. So, that’s the processing speed part of it. Then the other part is executive functioning. Executive functioning is the capacity to create sustained, monitor, regulate, goal-directed behavior. So, it’s when looking at the cognitive side of Lyme disease, it can be confused with Alzheimer’s. It can be confused with attention deficit disorder. It has unique qualities different from other cognitive impairments. In some ways it has more similarities to postconcussion syndrome.
With executive functioning, it’s hard to plan, prioritize, multitask. It’s hard to work and chew gum at the same time so to speak. Time management becomes poor. It’s hard to keep organized. People make careless mistakes. They [crosstalk 00:25:17] in the refrigerator and the milk in the cabinet. That goes with difficulty multitasking, getting sidetracked.
Then another part too can be the sensory hyperacuity, the excessive sensitivity to sound, light touch, smell, sometimes vibration. So, that there can be the sensory overload and the person deem it very flooded and emotionally react to the dog barking, noise and then they can’t hear themselves think. They get overwhelmed and then they become night owls, because only then can they hear themselves think. Then they stay up at night and they get sleep deprived. The sleep deprivation doesn’t help. So, all those things are a common vicious cycle of the disease progression that’s driven by these conditions.

Cindy K.: Now you just mentioned something that’s real important and we see a lot. My particular first symptom was a sleep disorder. I was waking 17 times that I could count at night but yet on a sleep study the sleep neurologist said to me, “You know what? You’re waking up like 30 times in an hour and I’ve never seen this before.” So, I was never getting restorative sleep. What cause that?

Robert B.: There’s a lot of different issues. Sometimes trouble falling asleep can increase the symptoms. There can be nightmares. There can also be … normally with healthy sleep, you get cycles of deep sleep in the beginning of the night which helps with your immune functioning. Then you get REM sleep towards early morning hours and then you’re recovered. One study looked at sleep patterns of Lyme patients and 100% of Lyme patients had sleep disorders. So, a lot of times one of the first things they attack is the sleep disorders.
Now I’ve also seen sleep apnea. It can be common. You can see narcolepsy with some patients. Cataplexy besides the nightmares. The anxiety and the depression that can be a part of Lyme disease can contribute to the sleep disorders. There’s multiple facets to it. So, it’s often can be … and the pain can be contributory. A person will lie in one position and we’re in pain. The pain interferes with their ability to sleep. So, the nonrestorative sleep when that perpetuates because sickness syndrome is often state where you curl up in a ball and you sleep and your body diverts it’s energy inside.
When that is effective, then it helps you recover, but if you’re never really sleeping, you’re never recovering. Sometimes getting the sleep better is more critical I think sometimes than antibiotics, because you play such in two ways. One is with narrowed immune system and the other is with whatever antibiotic a doctor thinks might work. Who’s smarter, your immune system or us as doctors trying to pick which antibiotic? An immune system is smarter. So, doing everything you can to help the body heal is a first step.

Cindy K.: What type of medicines are best for these people with sleep disorders since they’re so many of them and they affect the brain in a variety of different ways? What have you found to be the best to aid in sleep?

Robert B.: Well, all of your FDA approved sleep meds invariably help someone fall asleep and stay asleep longer, but none of the FDA except for one and that’s [inaudible 00:29:18]. None of the FDA approved sleep meds actually improve quality of sleep. So, by sleeping longer then there’s some improvement. So, there are certain meds particularly a couple of the antidepressants that we know improve deep sleep, sleep architecture. Those are sometimes one of the first things we try to distract them. Remeron, a couple of doxepin so those can promote more that deep sleep that is more critical, but of course you can’t have quality of sleep unless you also fall asleep. So, you want to look at can the person fall asleep, can they stay asleep, do they have an early-morning awakening and do they have good quality of sleep and then you break it down.
For instance, falling asleep is there trouble to turn of your head, is there trouble to calm down your emotions, is there difficulty relaxing your body, is there difficulty actually feeling sleepy and that would determine which approach we would take in treatment.

Cindy K.: We’re also battling adrenal issues and sometimes your time becomes your … you have such a hard time getting up in the morning and getting going and then you’re struggling. Then supper time happens and then all of a sudden you’re revving up.

Robert B.: That goes with the circadian rhythm. The theory there is you get the deep sleep and the deep sleep not only helps with immune functioning, but it also promotes the secretion of growth hormone which is the master hormone and help set circadian rhythm.

Cindy K.: Do you feel the severity of symptoms relate to the length of the time that they’ve been infected?

Robert B.: Yes. One of every occurs although you do see some people who have a very rapid progression of the symptoms. More commonly, when I see the psych symptoms, that’s usually a few years after infection. That doesn’t happen early. You can get brain fog. You can get some of the cognitive impairments earlier but the depression, the panic attacks, the various anxiety symptoms, aggressiveness, those things it usually several years later. A lot of times when people don’t make the connection, neuropathy, that’s often a later symptom. So, even though some people progresses quicker than others, my average patient that I see has been infected 5, 10, 15, 20 years sometimes longer.

Cindy K.: Yes. See, there’s just so much. A lot of people are unhealthy to begin with, because they’ve got other co-infections. I’m sorry no comorbidities such as diabetes or hypertension or cardiac especially as they get older. So, it can get most confusing. So, I do have one other question that I want to ask you. Then, I have a couple of other quick questions. In terms of the vascularity changes that happen, are people with Lyme more prone to have TIA which is a transient ischemic attack?

Robert B.: I haven’t seen that much although that may be more in Europe where there’s some .. one way to think of how Lyme affects the brain is where it’s neuroborreliosis in the brain, Lyme encephalopathy in the body affecting the brain and then the third way can be vascular. It does affect the vascular system. People can [inaudible 00:33:26] a part of that but when people have that vascular form, there’s vasculitis or it’s impacting the vasculature that some people for instance they get aneurysms. So, when they have that vascular form, I think it can but that does seem more common with European strains than what we see here. For some reason, in fact Carolina there’s what’s called the stroke belt. What is it in South Carolina where there’s more that there? You’d wonder is there a local pathogen that may be contributes to some vascular anomaly. Also with vascular disease, you can’t just think of Lyme. You could also think of dental spirochetes. That’s playing a role there chlamydia. So, it’s a number of other infections not just Lyme and looking vascular issues.

Cindy K.: Yeah. No wonder why this is so complicated. Well, I’ll tell you this has been a wonderful learning lesson from you. It’s very complex and we run the gamut of people having the sleep issues, the anxiety, the depression, the anger, the rage that can occur with this. So, again it’s very complicated and thank God for people like you that can invariably look at this at a whole different way. I know that you’re helping other people to understand this and teaching people to be open to this type of psychiatric neuro changes that can happen. So, now we’ve got a couple of fun things. Okay?

Robert B.: Okay.

Cindy K.: All right. So, what ticks you off?

Robert B.: What ticks me off? Okay.

Cindy K.: Got to be something.

Robert B.: I guess when someone has an answer before they even think about your question.

Cindy K.: Okay. I hope I didn’t do that.

Robert B.: [inaudible 00:35:39].

Cindy K.: I hope I didn’t do that.

Robert B.: No. I found that you can … I see relevant to Lyme disease where you think something and someone has like they don’t even think. They don’t process it. They have already made knee jerk answers without really thinking or the context. That’s part of why they end up in the controversy.

Cindy K.: Okay. That’s absolutely true. The second thing. So, I look at it. I had Lyme disease. Now I’m able to be a facilitator for education and that’s basically having lemons and turning it to lemonade. So, what has been your lemonade?

Robert B.: I wasn’t really looking for Lyme. Lyme kept finding me whether I wanted to deal with it or not. Being a doctor, I think it’s been very gratifying to help people and particularly helping people in ways where they otherwise would not have had help before. That’s a lot more gratifying than doing something that’s a rubber stamp assembly line part of medicine that anybody could do. So, I think it’s good to feel that I’ve had some impact on helping advance understanding in a piece of medicine that previously wasn’t well understood.

Cindy K.: I’ll tell you I hope that more people are going to think about this. I think that it’s unfortunate that the Lyme community is small. It’s not as broad. Medical schools aren’t really putting this as part of their education or it is but very limited. So, thank you so much for this talk, this interview. It’s been most enlightening. I hope that everyone out there listening has enjoyed Dr. Bransfield. He’s just super, super knowledgeable. I thank you and I want to say I hope that I meet you sometime soon. Again, thank you. You al-

Robert B.: Okay, thank you.

Cindy K.: Yes. You all have been listening to Living with Lyme another episode. This is Cindy Kennedy, nurse practitioner and I want to encourage you to reach out and subscribe to the website so you can stay connected Everybody have a great day. Come back and listen real soon.