Update On My Lyme Journey: Part 2

It's been over five months now since I started my new Lyme treatment. Despite working really hard for more than three years using various protocols, my doctor and I found out last September that I still have an active infection. 

Discouraging, but we also found out a significant missing piece to this puzzle in how the chronic Lyme infection has affected my immune system. To read my previous health update about this, please go here. 

I am having some rough days on this treatment; it's really up and down. Some days I feel better, other days I feel bad, and many days fall somewhere in-between. However, it sure beats feeling the absolute worst every day, all day, like I have for so many years.

We're also treating the long-term Epstein-Barr (EBV) infection I've struggled with for quite a while, too. Last fall, the immunologist that my doctor consulted said it's imperative to treat EBV in conjunction with Lyme because they get layered together and play off of each other. Therefore, treatment must target or address both. 

 Several years ago, I was treated by a physician for over two years with different prescription antivirals (Valtrex and Famvir) for Epstein-Barr specifically. Clearly, it didn't work because it's still an ongoing issue for me. However, we didn't know about the Lyme infection back then, so I believe Lyme and EBV do work in tandem, just as the immunologist said. Before hearing that from him, I'd always felt a link between them because of my own experience.

We are also working to correct the severe immune dysfunction the Lyme bacteria have caused in my body. I certainly think this has played a role in the chronicity of EBV, but I also believe Lyme disease directly has everything to do with keeping Epstein-Barr in a reactivated state.

As for the immune dysfunction, I'm stuck in overdrive on my T-helper 2 side, which means it overacts. As a result, this has pushed my T-helper 1 side into suppression, which causes it to underact. All of this is due to the chronic Lyme infection. It's been happening for a lot of years and has thrown me into an auto-immune cycle. The immunologist also told us long-term Lyme infections cause the immune system to become so confused that it literally loses its intelligence, but we're working to restore it.

I'm experiencing more neurological stuff at times, too. I've been having a lot of buzzing, tingling, numbness, burning, and shock-type pains. The sensation on the left side of my face was very dull for several days. All of these sharp, burning pains feel like touching an electric fence that sends a burning jolt through you. While it isn't very pleasant to go through, I think it's actually a sign my body is working to heal and repair my nervous system. I believe the treatment is helping reduce inflammation and better support my neuronal function, which is precisely what it's supposed to do. 

Also, the large Lyme ring rashes I've had on my back, chest, and abdomen for almost a year now are significantly better since starting this treatment. At one point, I seriously looked like I had the Olympic rings on my back, except there were way more than five. Overall, it has mostly cleared up, and I am so glad. A big thumbs up for that! 

I'm not sure what's coming next in terms of how I'll feel. It will probably oscillate back and forth, but either way, I've got to do this. We must deal with this Lyme infection as outright as possible and continue reducing inflammation in my body. I do believe there are some good changes are in progress. I just hope and pray I feel better sooner rather than later.

On a side note, this year, 2014, marks twenty years of chronic illness for me. I can't help but think back through the many long and difficult years and wonder how I've survived it all. It's been hard, and that's an understatement. But, as I've said many times before, and it really is true, God has kept me in ways only He could.

My beloved mother is and has been all throughout these years, my "boots on the ground," if you will. And let me tell you that when you're chronically ill, you need present, tangible help every day. 

Love and well wishes from afar are nice, but they aren't the present and tangible help you need when you're so profoundly sick, debilitated, and fatigued. She's the one who has been by my side through all of this, and I am ever grateful. I can't begin to tell you how much she has done for me over these past twenty years. Not only the big things but also the small day-in-day-out things. I am blessed by her care and devotion in helping me be well.

Prayer helps sustain us very much, but practical help is equally necessary; it takes both to get through this. Actually, when you're that sick and fatigued, and you can't function, you need those real and present hands and feet more than anything else. 

So yes, prayer helps, but it doesn't make meals for you or tangibly meet your ongoing physical needs each day. It doesn't drive you to doctor's appointments and sit with you while you're receiving your lab or test results. It doesn't hold your hand while you're having an awful day. In other words, love in action from somebody is required.   

My Mom and Dad have both made many sacrifices to help me since I've been ill. And I understand how truly blessed I am to have the ongoing support I do because many do not. My illness has been hard for my family too. I know it can't be easy to watch someone you love suffer so much for so long. Chronic illness truly affects everything.

What I'm experiencing while on this treatment isn't something I haven't already on some level over the years, but it sometimes gets wearisome. And, again, if you don't have that ongoing tangible support, it's doubly hard and stressful. 

Many do not have the support they need, and they suffer more as a result. Everyone whose sick should have somebody in their life they can depend on to help them, but sadly, that's not always the case. And that hurts my heart.

Let me say that I absolutely believe God is doing what only He can in this, but in the meantime, I have to keep doing what is necessary, too, and it is a full-time job. 

I continue asking Him for perseverance and resolve, so if you'd like to pray anything for me now, please pray for that. And please pray for everyone who has Lyme disease. The suffering is often so tremendous, and not everyone has a caregiver to help them regularly.

Better yet, if you know someone with Lyme, or any chronic illness for that matter (especially with no ongoing support), offer to help them practically in some way. For instance, offer to run errands or help around the house somehow. Perhaps they need transportation to an upcoming appointment, and, if you're able to do so, filling that void would sure lift a burden. Ask what their specific needs are and then follow through with the particular help.

I'll end for now by saying, none of this is easy, but you just have to focus on what needs to be done each day - that's what I've learned through the years.

Take one day at a time. 

Be brave. 

Do the work. 

Cry when you need to. 

And then trust God with the rest. 

Michelle

DesBio Lym Drops (Updated August 2014)

DesBio's homeopathic Lym drops (yes without the "e") have become such a helpful support in my overall Lyme treatment. It's not a cure all but I find it gives me some much needed relief; in particular it helps me when I'm having Lyme related headaches, eye sensitivity, and fevers. Not so much for fatigue.

Again this is not a stand alone treatment for chronic Lyme but rather a supportive therapy. Taking several drops three times a day yields the best results. But of course, each day is different and the benefits can last longer than others. So I take more drops at certain times than others. Some days, Lym is like a little miracle for me.

The point of all this being it helps to bring about some relief. And when you're suffering with a Lyme headache, ear pressure/fullness, sensitivity to light, fever or aching muscles and joints; any relief is welcome.

The deeper I go into treating my long term Lyme infection, the more I find I need this Lym homeopathic support. I honestly cannot be without these drops some days. When I don't take it, I suffer more; especially with headaches and light sensitivity. So I take it daily. Its as simple as that.

This is also great to have on hand for tick bites as you can apply drops directly to the site.

DesBio, short for Deseret Biologicals, makes many homeopathic, nutritional and botanical medicines. On a side note, they also make what are called Series Therapy kits for many different kinds of bacteria, viruses, etc. And they make one for Borrelia burgdorferi as well (which also includes Babesia). I treated with two of the different Borrelia Series Therapies (Basic and 1M) for over a year and it helped with certain things more than others. The biggest difference it made for me was in totally stopping a Lyme-related arrhythmia I had for two years prior to that time. My doctor and I didn't know Borrelia was at the root of the arrhythmia until it totally subsided after I started these potent homeopathic series therapies. That alone was huge!

I personally respond very well to homeopathic medicine. Certainly different things work for different people and I believe everyone has to do whatever works best for them. So anytime I find something that helps me in a significant way, I like to share it. And in sharing my own experience, I always hope it might be of help to someone else. If you've used Lym or any other DesBio products for Lyme disease, I'd love to hear if and how it's helped.

FYI: there are a few places online you can find this but otherwise; DesBio products are usually sold through healthcare professionals.

In love and hope,

~Michelle


*UPDATE - August 2014*

Desbio has recently changed LYM to Lyme Plus. The major difference is the adding of Babesia microti and Ehrlichia (thus the "Plus"), which makes this more comprehensive but is still different from the Series Therapies. I think it's a great formula to add as an aid to any Lyme disease treatment because many of us have Babesia and/or Ehrlichia infections as well. But remember; different things work for different people.

Hard Science On Lyme: Trials and Tribulations of Getting Borrelia Biofilms Accepted for Publication

Dr. Alan MacDonald, MD, shares an insightful, albeit frustrating article today on the blog, Hard Science On Lyme at LymeDisease.org. It goes along with my previous post of Dr. MacDonald's video interview on the biology of Lyme disease in which he discusses many things Lyme, including the role biofilms play in chronic Borrelia infections.

I've said it before and I'll say it again, as we in the Lyme community well know, Dr. MacDonald and Dr. Eva Sapi are audaciously leading the way in establishing the solid science of Lyme borreliosis. Eventually, the powers that be will have to acknowledge the truth of what they are scientifically proving.

I can't think of a more fitting quote right now than this one by Author Schopenhauer: "All truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. And third, it is accepted as being self-evident."

Thanks to LymeDisease.org for posting this article and always advocating for the truth of Lyme disease. The intro and link to the blog are below. ~ Michelle

In this guest blog, pathologist Alan MacDonald describes the struggle to publish the discovery of Borrelia biofilms and what the existence of these biofilms means for chronicity and treatment. Click here to read the full article.

The Biology of Lyme Disease: An Expert's Perspective

I wanted to share this informative interview (May 2013) with Dr. Alan MacDonald, MD, clinical pathologist and researcher. He explains the microbiology of Lyme (Borrelia spirochetes) disease and the connection he has found in his many years of research to degenerative neurological conditions, including Alzheimer's disease.

He starts by explaining some of his medical background and training and how he became interested in studying and researching spirochetal diseases, first with Syphilis (Treponema pallidum), and then more specifically, Lyme disease (Borreliosis).

Of note is an interesting case study regarding a German physician who had Alzheimer's disease. Dr. MacDonald and his team found high antibody levels of three different strains of Lyme spirochetes in his spinal fluid as well as Lyme spirochetes in his brain.

He also stated he could grow Lyme spirochetes from four Alzheimer's brains in his work with culturing brain tissues through the George Glenner Alzheimer's Brain Bank at the University of California at San Diego.

He discusses biofilms, DNA changes, and mutations of the Borrelia bacteria. During the last ten minutes, he eloquently explains why Lyme testing methods are flawed here in the USA. As many of us with Lyme already know, standard labs only test for one strain of Borrelia when testing for Lyme infection. At the same time, there are about 100 different genotypes of Borrelia burgdorferi (Bb) alone and many other species of Borrelia bacteria as well, i.e., B. afzelli, B. andersonii, B. microti, B. miyamotoi, etc.

Dr. MacDonald is a true pioneer in Lyme research, and his vast knowledge of Lyme disease biology is over-the-top excellent. He's done most of his work at Harvard and in his own basement. He's best known and beloved in the Lyme community for his role in the Lyme documentary, Under Our Skin.

At the filming of this interview, he stated that he now collaborates with Dr. Eva Sapi, Ph.D., in her ongoing Lyme research at the University of New Haven while also continuing his research in Alzheimer's and Lyme Neuroborreliosis. Two great scientific minds for sure!

I think that Dr. MacDonald has laid a solid foundation of research for the role Lyme spirochetes can play in many neurological diseases, including MS and ALS. Instead of calling Lyme "The Great Imitator," perhaps it should be called The True Root of Many Disease Processes more fittingly.

This video is just under thirty minutes. It's clearly worth watching if you have Lyme or someone you love does. I found it very interesting and enlightening. Also, it will prompt you to go directly to YouTube to watch.

Love and blessings,
Michelle

P.S. If you're interested in reading more about the microbiology of Lyme, Borrelia bacteria, or how it affects the immune system and other cells, consider reading The Complexities of Lyme Disease by Thomas Grier, MS which is also excellent. Click here to read Part 1 or find the whole series listed in my blog archive under March and April 2013.

iSpot Lyme: New Generation of Testing From NeuroScience, Inc.

NeuroScience, Inc recently anounced the release of a new, and suppossedly more sensitive, Lyme test called iSpot Lyme (TM).

NeuroScience states that iSpot Lyme has a sensitivity of 84% and specificity of 94% for the detection of Borrelia burgdorferi (Bb); making it an excellent complement to the current two-tiered antibody method of testing.

"The iSpot Lyme detects a cellular immune response against Lyme antigens, which appears earlier in the disease process (2 weeks) than the antibody response detected by the traditional Western Blot test (4-6 weeks). More importantly, iSpot Lyme can even detect antigen-specfic T cell response in seronegative patients" (iSpot Lyme: A New Approach to Lyme Disease Testing - The NEI Connection).

If this pans out, perhaps it will be the start of a new direction in better testing methods that will be more accurate and more widely available (being the standard and not the exception). And maybe it will lead to effectively testing for other strains of Borellia as well. That is much needed also. 

I've had good experiences in the past with other types of testing through NeuroScience (Pharmasan Labs). I think they hold a high standard in neurotransmitter testing. Perhaps they'll become a new high standard in accurate Lyme testing too. Let's hope so.

To read more about this new testing method check out iSpot Lyme: A New Approach to Lyme Disease Testing on The NEI Connection blog.

For more detailed information read the White Paper and download the PDF iSpot Lyme (TM): A New Generation of Lyme Disease Testing

When peripheral blood mononuclear cells (PBMCs) from a B. burgdorferi-infected patient are exposed to B. burgdorferi protein antigens (A) B. burgdorferi-specific T cells are activated and secrete small proteins called cytokines (B) T cells that are not specific for B. burgdorferi do not become activated. iSpot Lyme (TM) measures the cytokine IFN-gamma secreted by the patient's T cells. Cytokine proteins (IFN-gamma) are captured near the cells that secreted them and are then detected using a color reagent (C).

Lyme Disease Awareness Month

It's May, and that means Lyme disease awareness month. Lyme is caused by the spirochetal bacteria Borrelia burgdorferi (Bb) transmitted through the bite of an infected tick. Lyme is primarily a tick-borne infection. However, transmission is also possible through infected mosquitoes, fleas, and other insects. 

Lyme disease is not to be taken lightly. If left untreated or not treated sufficiently, it can disseminate throughout the body, damaging cells, organs, and tissues. It is a multi-system disease, meaning it affects many systems in the body. Long-term or chronic Lyme can significantly affect the heart, joints, muscles, nervous (central and peripheral), and immune systems. It has been documented that the Bb bacteria can invade the brain within the first 48-72 hours of infection. Lyme disease is also known as "the great imitator" because it can mimic other diseases and illnesses. Accurate diagnosis is paramount. 

Remember ticks also often carry other serious pathogens such as Bartonella (Cat Scratch Fever), Babesia, Ehrlichiosis, Rocky Mountain Spotted Fever, Relapsing Fever, Q Fever, Tularemia, and Powassan virus. This speaks of the more common picture of Lyme disease today, which is chronic, relapsing, and includes multiple co-infections, such as those listed above, and other viruses, parasites, and fungals. This is more appropriately termed the Lyme disease complex. I'll be writing more about this throughout the month, the life stages of ticks, and how to properly recognize and remove them. 

We are now entering the season that ticks are most active (mid-Spring to Fall). So please be mindful to check yourself, your kids, and pets for ticks after being outdoors. And don't forget to check those inconspicuous places like belly buttons, underarms, in and behind ears, between toes, and groan areas. 

Educate yourself. Please see What Is Lyme Disease? for more detailed information about risk factors, safety precautions, and the symptoms and stages of Lyme. 

Please see Resources for a list of helpful websites, blogs, and books related to Lyme, co-infections, and other relevant health issues. 

You might also want to consider reading The Complexities of Lyme Disease series by Thomas Grier, M.S. Part 1 can be found here, or the entire series is listed in my blog archive (March and April 2013).

Michelle 

The Complexities of Lyme Disease (Part 4): Lyme Receptors

This is Part 4 in the series The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1. Here to read Part 2. And here to read Part 3.

Lyme Receptors 

It now appears that there are specific receptors in the Lyme spirochete to attach to endothelial
cells, N-Acetyl-glucasomine, B-cells, glial cells, nerves, and neurons.

The way our immune system is supposed to work is that it recognizes foreign invaders as being different from self, and it attacks the infection. Unfortunately, the immune system sometimes attacks our own cells. This is called autoimmune disease. If a foreign invader has a chemical structure similar to our own tissue antigens, our bodies sometimes make antibodies against our own tissues. In people with Lyme disease, scientists have discovered auto-antibodies against our own tissues, including:

• Nerve Cells (Axons)
• Cardiolipin 
• Myelin (also seen in MS)
• Myelin Basic Protein (also seen in MS)
• Neurons (brain cells)

When the immune system finds a foreign invader, it tags that invader in a number of ways. A cell called the macrophage can engulf the bacteria and then communicate to other immune cells the exact description of the bacteria. Another cell might mark the cell with an antibody, which attracts killer T-cells. Some types of T-cells communicate to other cells what to attack and regulates the immune assault. But sometimes, the body can produce a type of antibody that doesn't attack or help. A blocking antibody will attach and coat the intruder, but it won't fix *compliment, and it shields the bacteria from further immune recognition. In Lyme, we have seen quantities of IgG4 blocking antibody such as is seen in some parasitic infections (Tom Schwann RML 92 LDF Conference).

[* Note: Compliment is a term used for a series of 18 + digestive proteins that are only activated by signals from our immune system, such as complement-fixing antibodies that attach to foreign antigens.]

In order for the immune system to make an attacking antibody, the immune system must first find an antigen that it can attack. Unfortunately, as seen by freeze-fracture electron microscope, photographs of the Lyme bacteria show that most of the antigens are on the inside of the inner membrane and not on the outside. This makes the bacteria less visible to the immune system and more difficult to attack.

The most intriguing fact about Borrelia spirochetes is their well-documented ability to change the shape of their surface antigens when they are attacked by the human immune system. When this occurs, it takes several weeks for the immune system to produce new antibodies. During this time, the infection continues to divide and hide. It appears that Borrelia are able to change their surface antigens many times and can do it quickly.

Borrelia burgdorferi (Bb) correlates with the enhancement of Toll-like 

receptor 2 (TLR2) expression by microglia 

American Society for Microbiology

In one study by Dr. Andrew Pachner, M.D., he infected mice with a single strain of Borrelia burgdorferi. After several weeks he was able to isolate two slightly different forms of the bacteria. The bacteria from the bloodstream was attacked and killed by the mouse's immune sera, but the bacteria isolated from the mouse's brain was unaffected by the immune sera. The bacteria isolated from the mouse's brain had a new set of surface antigens.

It appears that contact with the CNS caused the bacteria to change its appearance. Since the brain is isolated from the immune system and is an immune-privileged site, the bacteria became its own separate strain.

This means: Infections of the bloodstream may be different from the infections that are sequestered in the brain. While we continue to have active immunity in the bloodstream, the brain has no immune defenses except for circulating antibodies. So if those circulating antibodies are ineffective to attack the bacteria in the brain, then the brain is left without any defenses, and the infection goes unabated.

Another peculiar observation of this bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin), the bacteria start to produce bacteriophage.

A phage is a virus that specifically attacks bacteria. In this case, there are two distinct forms. This means the Lyme bacteria at one time was attacked by viruses; it was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients?

The Complexities of Lyme Disease ( A Microbiology Tutorial) by Thomas Grier, M.S.

The Complexities of Lyme Disease (Part 3): When Lyme Bacteria Infects the Brain

This is Part 3 of the series, The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1 and here to read Part 2. Part 4 is soon to come.  ~ Michelle

When Lyme Bacteria Infects The Brain:

As we have previously discussed, the pathogen that causes Lyme disease is a highly motile spirochete within the Borrelia family of bacteria. This is the same group of bacteria that cause Relapsing Fevers in Africa and around the world. Like other Relapsing Fever bacteria, Borrelia burgdorferi (Lyme bacteria) has both an affinity for the brain and a mechanism to penetrate into it.

While Lyme may be a bit more subtle upon penetrating the brain, its silent but insidious invasion may be the reason that brain involvement can and is often overlooked by physicians for months or even years in neurological Lyme patients.

In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite of an infected tick to the brain in just a few days. While we know this bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect.

When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood-brain barrier (e.g., IL-6, Tumor Necrosis Factor-alpha, IL-1, Transforming Growth Factor-beta, etc.). In addition to affecting the blood-brain barrier, these cytokines can make us feel ill and give us fevers.

Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can’t enter either, making treatment of the brain especially hard.

For the first ten days of a Lyme infection, the blood-brain barrier (BBB) is virtually nonexistent. This not only allows the Lyme bacteria to get in but also immune cells that can cause inflammation of the brain.

* Note: The breakdown of BBB was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive iodine. The CSF (cerebrospinal fluid) of mice was tested, and then they were infected with Bb (Borrelia burgdorferi). The CSF was then retested every day after for several weeks. The result? No crossover of iodine was present in the control group, but 100% crossover was in the infected group for 10 days. The infection had the same result on the BBB as if you were injecting the radioactive iodine directly into the brain.

Once the Lyme bacteria enter the brain, they continue to divide and become entrenched within the brain's tissues and cells. Borrelia burgdorferi is directly neurotoxic upon contact with neurons and also has a negative effect on glial cells trying to repair brain injury. This, in turn, further increases the permeability of the blood-brain barrier, allowing, even more, blood-borne agents to enter the brain. The immune system responds to the new flood of internal bacterial antigens and produces more inflammatory cytokines. The result can cause brain edema or encephalitis, intracranial pressure, and focal areas of demyelination.

Also, when the human brain becomes inflamed due to infection with the Lyme bacteria, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson’s Disease, MS, and ALS. What quinolinic acid does is to stimulate neurons to repeatedly depolarize. If this goes on unabated, it eventually causes the neurons to demyelinate and die. Basically, people with elevated quinolinic acid have short-term memory problems.

This means: If we think of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can’t learn anything. If all of the lines going out are busy, we can’t recall any memories. Our thinking process becomes impaired.

A second impairment to clear thinking that Lymies can experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computerized Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal “Swiss-Cheese” pattern of blood flow. The cortical or thinking region of the brain was being deprived of good circulation, while the occipital (eyesight) regions had an increased flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes.

The Complexities of Lyme Disease (A Microbiology Tutorial) by Thomas Grier, M.S.
Neurocascade Events and Lyme by Thomas Grier, M.S.

The Complexities of Lyme Disease (Part 2): Motility of the Lyme Bacteria

This is Part 2 of the series The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1. I'll post Part 3 next week.  ~ Michelle

Motility of the Lyme Bacteria: 

How does the Lyme bacteria travel from the bloodstream to other tissues? While we have known for a long time that the Lyme spirochetes can show up in the brain, eyes, joints, skin, spleen, liver, GI tract, bladder, and other organs, we didn't understand the mechanism by which it could travel through capillaries and cell membranes. Then, Dr. Mark Klempner, M.D., presented at the 1996 LDF International Lyme Conference an interesting paper that gave us part of the answer.

Many researchers have observed that the Lyme spirochete attaches to the tip of the human cells first. It then wiggles and squirms until it enters the cell. What Dr. Klempner showed was that when the spirochete attached to the human host cell, it caused that cell to release digestive enzymes that would dissolve the cell and allow the spirochete to go where ever it pleases. This is very economical for the bacteria to use our own cell's enzymes against us because it does not need to carry the genes and enzymes around when it travels.

Dr. Klempner also showed that the spirochete could enter cells such as the human fibroblast cell (the skin cell that makes scar tissue) and hide. Here the pathogen was protected from the immune system and could thrive without assault. More importantly, when these Bb-fibroblast cultures were incubated with Rocephin (ceftriaxone), two-thirds of the cultures still gave rise to live spirochetes after two weeks and in later experiments for more than 30 days.

If we can't kill it in a test tube at these high concentrations of Rocephin in four weeks, how can we hope to kill it in the human body?

This means: The infection can enter the best tissue that is optimal for its survival. Once it gains an intracellular position, it may evade the immune system and antibiotic therapy by remaining sequestered away from these hostile environs.

Another interesting observation about this bacteria is how it interacts with our body's immune system.

Dr. David Dorward of the NIH Rocky Mountain Laboratories showed that when healthy normal human B-cells were placed in a culture with live Borrelia burgdorferi, it was only a matter of moments before the spirochetes started to attach and penetrate the antibody-producing white blood cells. Once inside the cell, the bacteria should be killed by a process wherein B-cell lysosomal enzymes dissolve the bacteria. But this does not happen. Instead, the bacteria actually thrive and eventually destroy the lymphocyte.

What is much more disconcerting is that by using a time-lapse video camera, the spirochete can be seen to enter the B-cell and exit a short distance later. But when it exits, it appears to be wearing the membrane of the B-cell. The live motile bacteria then swims about unharmed in the sea of B-cells because by wearing the cloak of its enemy, it goes undetected. This stealth-type camouflage will prevent antibodies from attaching to it; it prevents the complement enzymes in the blood from finding and destroying it, and it eludes the scavenger white blood cells such as macrophages and killer T-cells that normally hunt and destroy foreign pathogens.

This means: We have a highly evolved bacteria that is highly mobile, can dissolve any tissue it desires so it can find immune-privileged sites, and can camouflage itself from our own immune system by wearing the membrane of the very cells that are supposed to track it down and kill it. This bacteria seems to have evolved a sophisticated defense mechanism to avoid our immune system.

Lyme bacteria (Borrelia burgdorferi spirochete) in human blood

The Complexities of Lyme Disease (A Microbiology Tutorial) By Thomas Grier, M.S.

The Complexities Of Lyme Disease (Part 1): The Structure of the Lyme Bacteria

I recently came across this fantastic excerpt written by Lyme researcher and lecturer, Thomas Grier, M.S., who was misdiagnosed with M.S. for years when he had chronic relapsing Lyme disease. Sounds familiar to many of us, I know. He is now the Executive Director of Pathology Studies at MIBDEC (Minnesota Insect-Borne Disease Education Counsel), a non-profit organization. He has a background in microbiology and immunology and continues to do research in both the Lyme and M.S. communities. 

The article is so long that I'm breaking it into parts and using excepts that might not be as well known or understood. I found it extremely interesting. While I already knew some of the basic information; it truly helped me better understand the complexities of Borrelia (Bb) and its effect on and within the human body. I felt the need to share it.

Perhaps some of you are familiar with Grier and/or his work. I had previously read his personal story a couple years ago but never knew he had written the manual (Lyme Disease Survival Manual) this excerpt is taken from. 

I'll post Part 2 in a week or so but I've included a link to the full article at the end of this post for those who want to read it in it's entirety now.    ~ Michelle

Excerpts from The Complexities of Lyme Disease 

by Thomas Grier, M.S.

Why is Lyme disease such a mystery? Why does it mimic so many other diseases? Why is it so difficult to detect? The reasons come from the microbiology of the bacteria that causes Lyme. This paper will look at the biology of this bacteria and the consequences of the organism's unique microbiology on human victims.

Lyme disease is caused by a spiral-shaped bacterium known as a spirochete. Diseases that are caused by spirochetes are notorious for being relapsing in nature, difficult to detect, and great imitators of other diseases. Syphilis, Tick-Borne Relapsing Fever, and Leptospirosis are other examples of spirochetal diseases. Lyme disease is caused by a bacteria called Borrelia burgdorferi, named after the man who isolated it from a Deer Tick in 1981, Dr. Willy Burgdorfer. The following is a tutorial to help explain away the mysteries of this bacteria, and why it causes so much controversy between patients and the medical community.

The Structure of the Lyme Bacteria:

The structure of the Lyme spirochete is unlike any other bacteria that has ever been studied before. It is one of the largest of the spirochetes (0.25 microns x 50 microns). It is as long as a fine human hair is thick. Borrelia burgdorferi is a highly motile bacteria. It can swim extremely efficiently through both blood and tissue because of internal propulsion. It's propelled by an internal arrangement of flagella, bundled together, that runs the length of the bacteria from tip to tip.

Like other Borrelia bacteria, Borrelia burgdorferi (Bb) has a three-layer cell wall which helps determine the spiral shape of the bacteria. What makes this bacteria different from other species is that it also has a clear gel-like coat of glycoproteins that surround the bacteria. This extra layer is sometimes called the Slime Layer or S-layer.

This means: This extra layer of glycoproteins (exaggerated in thickness here) may act like a stealthy coat of armor that protects and hides the bacteria from the immune system. The human immune system uses proteins that are on the surface of the bacteria as markers and sends attacking antibodies and killer T-cells to those markers called outer surface protein antigens (OSP antigens). This nearly invisible layer is rarely seen in washed cultures but can be seen regularly in tissue biopsies.

The Lyme bacteria is also different from other bacteria in its arrangement of DNA.

Most bacteria have distinct chromosomes that are found floating around inside the cytoplasm. When the bacteria starts to divide, it forms a new cell wall in the middle and begins to split in two. The chromosomes also divide, and the new copies of the chromosomes enter the new cell. The arrangement of DNA within Borrelia burgdorferi, however, is radically different from other bacteria. It is arranged along the inside of the inner membrane of the cell. It looks something like a net embedded just underneath the skin of the bacteria.

This means: We really don't understand the mechanisms of how Bb regulates its genetic material during its division. The bacterial DNA is uniformly embedded inside the inner membrane of the Bb bacteria, like nylon stocking.

Another unique feature to Borrelia burgdorferi are Blebs. This bacteria replicates specific genes and inserts them into its own cell wall, and then pinches off that part of its cell membrane and sends the Bleb into the host. Why it does this, we don't know? But we do know that these blebs can irritate our immune system.

Dr. Claude Garon of Rocky Mountain Laboratories has shown that there is a precise mechanism that regulates the ratio of the different types of blebs that are shed. In other bacteria, the appearance of blebs often means the bacteria can share genetic information between themselves. We don't know if this is possible with Borrelia species.

There have been reports of a granular form of Borrelia, which can grow to full size, fully autonomous spirochetes and can reproduce. These granules are so small that they can be filtered and separated from live adult spirochetes by means of a micropore filter. The granular/spore form of Borrelia burgdorferi is still being debated. (Stealth Pathogens Lida Mattman Ph.D. 66, Phillips/Mattman 98, Preac-Mursic)

The division time of Borrelia burgdorferi is very long. Most other pathogens, such as Streptococcus or Staphylococcus, only take 20 minutes to double. The doubling time of Borrelia burgdorferi is usually estimated to be 12-24 hours. Since most antibiotics are cell wall agent inhibitors, they can only kill bacteria when the bacteria begins to divide and form new cell walls.

This means: Since most antibiotics can only kill bacteria when they are dividing, a slow doubling time means less lethal exposure to antibiotics. Most bacteria are killed in 10-14 days of antibiotics. To get the same amount of lethal exposure during new cell wall formation of a Lyme spirochete, the antibiotic would have to be present 24 hours a day for 1 year and six months!

If a bacteria is in a non-metabolic state (dormant), no antibiotic is effective. To be lethal, the antibiotic must be absorbed and processed through the bacteria's metabolic machinery and cause a disruption of metabolism.

Unlike antiseptics, antibiotics don't kill on contact. If there are any dormant bacteria hidden in sequestered sites, then regardless of the length of treatment, antibiotics can fail until the bacteria become metabolically active (The Forgotten Plague see reference to Tuberculosis).

Like other spirochetes, such as those that cause Syphilis, the Lyme spirochete can remain in the human body for years in a non-metabolic state. We know this because patients with ACA rash for years are often culture positive when the skin is biopsied and cultured. Non-metabolic bacteria is essentially suspended animation. The bacteria does not metabolize in this state. Antibiotics are not absorbed or effective. When the conditions are right, those bacteria that survive can seed back into the bloodstream and initiate a relapse. It is a beautiful and patient survival mechanism.

This means: Just because a person is symptom-free for long lengths of time doesn't mean they aren't infected. It may simply be a matter of time before the re-emergence of the sequestered non-metabolic bacteria. Whereas viral infections often impart a lifelong immunity and may suppress subsequent relapses or reinfections, Lyme, like other bacterial infections, does not impart an active immunity for a long period of time. People are often reinfected with Lyme. A relapse of symptoms could actually be thought of as reinfection or a reseeding of infection from immune-privileged sites.

The Lyme spirochete has a sequence of surface antigens it can choose to express or not express. There are more than two dozen species of Relapsing Fever Borrelia bacteria that have been clearly identified. We are now beginning to see a similar diversity within the Lyme spirochete family as well. Polymorphism, which is the ability of the bacteria to change its structural identity, makes recognition and identification more difficult. It is like a criminal putting on a new disguise after every time he has committed a new crime.

While there are four generally accepted genospecies of Lyme disease - Borrelia burgdorferi, Borrelia afzellii, Borrelia garinii, and Borrelia lonstarrii - there are hundreds of identified strains of the first three species. Borrelia spirochetes are polymorphic because they have built-in genetic mechanisms to vary their antigens.

This means: Just as the immune system recognizes the bacteria and tries to kill it, the bacteria changes its clothes and fools the immune system, and survives a little longer. Soon the bacteria finds safer areas of the body to hide in, and the immune system stops looking for it. But another aspect of polymorphism is that once the cell changes, it may become even more lethal to some cells. For example, when Borrelia burgdorferi was introduced into the mouse via the bloodstream, the bacteria traveled to the brain. But the bacteria recovered from the brain was more adapted to the brain and could no longer be killed from antibodies in the bloodstream. Polymorphism is a clever way to survive and may offer reasons for multiple symptoms.

The Complexities of Lyme Disease (A Microbiology Tutorial) By Thomas Grier, M.S.

Borrelia burgdorferi (Bb) bacteria (spirochetes) magnified using dark-field microscopy.

Recent Lyme Disease Research News And Breakthroughs: Part 1

Some interesting and hopeful news has emerged from the medical establishment over the past two years concerning breakthroughs and open doors in Lyme research. This is hard science and not just speculation concerning Lyme disease. Big steps forward.

Many of you are already well aware of these to some degree, as we are a very informed group. Nevertheless, I wanted to post this information for those who might not yet know or have had the opportunity to read it. I also want to document some of these together in one place, if only for myself. There are clearly many past and present Lyme studies that are of importance. Of the recent studies I've found, I'm posting four of the ones I think to be quite significant. 

1.) Dr. Benjamin Luft, M.D., professor at Stony Brook University Medical Center in New York, and a team of fellow researchers, determined the genetic blueprint of 13 strains of the Lyme bacteria, Borrelia burgdorferi (Bb) in 2010 and posted their findings in the Journal of Bacteriology. 

The team wanted to identify why certain strains are more invasive than others, which was the motive of the study. Determining all of the Bb genome sequences will lead to understanding every organism's characteristics, advancing the foundation of better detection, treatment, and prevention.

Click here to read the October 2010 article Genetic Blueprint of Bacteria Causing Lyme Disease Unraveled on Phys.org.

Click here to read the article Genetic Blueprint of Lyme Disease Uncovered posted on Stony Brook University Happenings. 

2.) Dr. Steven Schutzer, M.D., an immunologist at the University of Medicine and Dentistry of New Jersey, uncovered biomarkers for Lyme disease symptoms that persist even after treatment. In the study, he examined cerebrospinal fluid samples from patients with Persistent Lyme and Chronic Fatigue Syndrome. After removing common proteins in the fluids, he documented different sets of proteins unique to each group. This is significant in that speculation has been removed concerning the differences between CLD and CFS.  

Click here to read Discover Magazine's January 2012 article Top 100 Stories of 2011: #90 Chronic Lyme Patients Validated. 

Click here to read the 2011 research article Distinct Cerebrospinal Fluid Proteomes Differentiate Post Treatment Lyme Disease from Chronic Fatigue Syndrome published in PLOS ONE. 

3.) Dr. Eva Sapi, Ph.D., associate professor in the Department of Biology and Environmental Sciences at the University of New Haven in Connecticut, just published research this past October in the Public Library of Science ONE (PLOS ONE) concerning biofilm colonies and their ability to protect Borrelia burgdorferi (Bb), the Lyme bacteria, from antibiotic therapy.

Sapi also published research in May 2011 concerning culture techniques, the sensitivity of the various forms of Bb, and the persistence of infection. The study demonstrated the ability of Bb to convert from spirochete to cyst form and the development of biofilm colonies of the Lyme bacteria. 

All of this research would clearly help explain the frequency of treatment failure and the persistence and reoccurrence of Lyme infection months or years after treatment. 

Click here to read the October 2012 article UNH Prof Closes In On Lyme Disease Breakthrough in The New Haven Register.

Click here to read the October 2012 research article Characterization of Biofilm Formation by Borrelia burgdorferi In Vitro published in PLOS ONE.

Click here to read the original research study article Evaluation of In-Vitro Antibiotic Susceptibility of Different Morphological Forms of Borrelia burgdorferi published in the Journal of Infection and Drug Resistance in May 2011.

Click here to read the May 2011 article posted on LymeDisease.org.

4.) Dr. Steven Norris, Ph.D., vice chair for research in the Department of Pathology and Laboratory Medicine at the University of Texas Health Medical School, along with fellow U.T. researchers, developed a new technique that allowed them to test 15 times more bacterial genes than in the previous thirty years. This advanced technology is expected to lead to an efficient assessment of the roles of Borrelia burgdorferi (Bb) genes in the infectious cycle and development of Lyme disease. Their findings were recently posted in October in PLOS ONE.

Click here to read the October 2012 article Scientists Step Up Hunt for Bacterial Genes Tied to Lyme Disease posted on Science Daily.

Click here to read the October 2012 research article Analysis of An Ordered Comprehensive STM Mutant Library in Infectious Borrelia burgdorferi: Insights Into the Genes Required for Mouse Infectivity published in PLOS ONE.

P.S. I believe more discoveries and breakthroughs in this next decade will lead to better treatment options. I'm praying for it, and I am praying for those dedicated scientists and researchers who are diligently working towards this end. They need wisdom, understanding, and funding. Let's pray for the resources they need. And let's hold onto this hope together.

Michelle